Updated on 2026/03/14

写真a

 
MATSUMOTO YOSHIHISA
 
Organization
Institute of Integrated Research Laboratory for Zero-Carbon Energy Professor
Title
Professor
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News & Topics

Degree

  • Master of Science ( The University of Tokyo )

  • Doctor of Science ( The University of Tokyo )

Research Interests

  • 放射線感受性

  • 放射線応答

  • 放射線影響

  • 温熱療法

  • DNA依存性プロテインキナーゼ

  • DNA二重鎖切断

  • DNA修復

  • Protein Phosphorylation

  • Antibody

  • Radiation Response

  • Radiation Effect

  • Hyperthermia

  • Cancer Therapy

  • DNA-dependent Protein Kinase

  • DNA Double-strand Break

  • DNA Repair

  • Radiosensitivity

  • がん治療

  • タンパク質リン酸化

  • 抗体

Research Areas

  • Environmental Science/Agriculture Science / Radiation influence

  • Environmental Science/Agriculture Science / Chemical substance influence on environment

  • Life Science / Molecular biology

  • Life Science / Radiological sciences

Education

  • The University of Tokyo   Graduate School of Science   Department of Biochemistry and Biophysics, Ph.D Course

    1995.4 - 1998.3

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    Country: Japan

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  • The University of Tokyo   Graduate School, Division of Science   Department of Biochemstry and Biophysics

    - 1998

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  • The University of Tokyo   Graduate School of Science   Department of Biochemistry and Biophysics, Master Course

    1993.4 - 1995.3

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  • The University of Tokyo   School of Science   Department of Biochemistry and Biophysics

    1991.4 - 1993.3

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  • The University of Tokyo   College of Arts and Sciences

    1989.4 - 1991.3

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Research History

  • Institute of Science Tokyo   Institute of Integrated Research, Laboratory for Zero-Carbon Energy   Professor

    2024.10

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  • Tokyo Institute of Technology   Institute of Innovative Research, Laboratory for Zero-Carbon Energy   Professor

    2022.4 - 2024.9

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  • Tokyo Institute of Technology   Institute of Innovative Research, Laboratory for Zero-Carbon Energy   Associate Professor

    2021.6 - 2022.3

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  • Tokyo Institute of Technology   Institute of Innovative Research, Laboratory for Advanced Nuclear Energy   Associate Professor

    2016.4 - 2021.5

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  • Tokyo Institute of Technology   Research Laboratory for Nuclear Reactor   Associate Professor

    2007.4 - 2016.3

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  • Tokyo Institute of Technology   Research Laboratory for Nuclear Reactor   Associate Professor

    2006.12 - 2007.3

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  • -:Tokyo Institute of Technology Research Laboratories for Nuclear Reactors Associate Professor

    2006

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  • :The University of Tokyo Graduate School of Medicine, Center for Disease Biology and Integrative Medicine Assistant Professor

    2003 - 2006

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  • The University of Tokyo   Graduate School of Medicine, Center for Disease Biology and Integrative Medicine, Department of Radiation Research   Associate Professor

    2003 - 2006

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  • The University of Tokyo   Graduate School of Medicine, Department of Radiation Oncology   Assistant Professor

    1998.5 - 2003.3

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  • :The University of Tokyo Graduate School of Medicine, Department of Radiation Oncology Assistant Professor

    1998 - 2003

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  • Japan Society for the Promotion of Science   Predoctoral Research Fellow

    1996.5 - 1998.3

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  • :Japan Society for the Promotion of Sciences Special Research Fellow

    1996 - 1998

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Professional Memberships

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Papers

  • Live-cell imaging of DNA damage and cell cycle progression uncovers distinct responses during neural differentiation of hiPSCs

    Mikio Shimada, Yoshihisa Matsumoto, Kensuke Otsuka

    Journal of Biological Chemistry   2025.7

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jbc.2025.110328

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  • Integrated Network Analysis Decipher ZNF384‐Related miR‐20b‐5p and miR‐424‐5p in Colon Adenocarcinoma

    Bo Zhang, Yoshihisa Matsumoto

    Cancer Reports   2025.5

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    Authorship:Last author, Corresponding author   Publishing type:Research paper (scientific journal)  

    DOI: 10.1002/cnr2.70233

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  • Antioxidants Ameliorates Ionizing Radiation-Induced Microcephaly in Cerebral Organoid Derived from Human-induced Pluripotent Stem Cells. International journal

    Mikio Shimada, Yoshihisa Matsumoto

    Radiation research   2025.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    Ionizing radiation exposure induces DNA damage and chromosome aberrations through both direct and indirect effect. The indirect effects are primarily mediated by the generation of hydroxyl radicals, a process attributed to radiation. Dimethyl sulfoxide (DMSO) and ascorbic acid (AA) are known as radical scavengers and have radioprotective effects. Radiation therapy is widely employed in the treatment of malignant tumors such as glioblastoma; however, its side effects, including cognitive impairments resulting from damage to healthy neurons, pose significant challenges. To ameliorate these effects, radioprotective reagents have been sought. In this study, we used cerebral organoids derived from human-induced pluripotent stem cells to address the radioprotective effect of radical scavengers, DMSO and AA in brain exposure. Although exposure to radiation for 20-day-old cerebral organoids results in DNA double-strand breaks and apoptosis leading to microcephaly phenotype, treatment with DMSO or AA not only before but also after radiation alleviated DNA damage, cell death, and the microcephaly phenotype. Our results suggest that DMSO and AA are candidates for the radioprotective reagents for brain tumor therapy.

    DOI: 10.1667/RADE-25-00017.1

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  • Radiobiological characterization of neutron irradiation field of UTR-KINKI for the research utility toward boron neutron capture therapy: Cell killing effect and its enhancement by 4-borono-L-phenylalanine

    Shoji Imamichi, Yoshihisa Matsumoto, Toshiro Matsuda, Satoshi Nakamura, Mikio Shimada, Hirokuni Yamanishi, Mitsuko Masutani, Minoru Suzuki

    Progress in Nuclear Science and Technology   7   377 - 380   2025.3

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    Authorship:Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:The Atomic Energy Society of Japan  

    DOI: 10.15669/pnst.7.377

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  • CDK-mediated phosphorylation of PNKP is required for end-processing of single-strand DNA gaps on Okazaki fragments and genome stability

    Kaima Tsukada, Rikiya Imamura, Tomoko Miyake, Kotaro Saikawa, Mizuki Saito, Naoya Kase, Lingyan Fu, Masamichi Ishiai, Yoshihisa Matsumoto, Mikio Shimada

    eLife   14   2025.3

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    Publishing type:Research paper (scientific journal)   Publisher:eLife Sciences Publications, Ltd  

    Polynucleotide kinase phosphatase (PNKP) has enzymatic activities as 3′-phosphatase and 5′-kinase of DNA ends to promote DNA ligation and repair. Here, we show that cyclin-dependent kinases (CDKs) regulate the phosphorylation of threonine 118 (T118) in PNKP. This phosphorylation allows recruitment to the gapped DNA structure found in single-strand DNA (ssDNA) nicks and/or gaps between Okazaki fragments (OFs) during DNA replication. T118A (alanine)-substituted PNKP-expressing cells exhibited an accumulation of ssDNA gaps in S phase and accelerated replication fork progression. Furthermore, PNKP is involved in poly (ADP-ribose) polymerase 1 (PARP1)-dependent replication gap filling as part of a backup pathway in the absence of OFs ligation. Altogether, our data suggest that CDK-mediated PNKP phosphorylation at T118 is important for its recruitment to ssDNA gaps to proceed with OFs ligation and its backup repairs via the gap-filling pathway to maintain genome stability.

    DOI: 10.7554/elife.99217

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    Other Link: https://cdn.elifesciences.org/articles/99217/elife-99217-v1.xml

  • Dimethyl Sulfoxide Attenuates Ionizing Radiation-induced Centrosome Overduplication and Multipolar Cell Division in Human Induced Pluripotent Stem Cells. International journal

    Mikio Shimada, Ryoichi Hirayama, Yoshihisa Matsumoto

    Radiation research   202 ( 4 )   719 - 725   2024.10

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    Language:English   Publishing type:Research paper (scientific journal)  

    Centrosomes are important organelles for cell division and genome stability. Ionizing radiation exposure efficiently induces centrosome overduplication via the disconnection of the cell and centrosome duplication cycles. Over duplicated centrosomes cause mitotic catastrophe or chromosome aberrations, leading to cell death or tumorigenesis. Pluripotent stem cells, including embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), can differentiate into all organs. To maintain pluripotency, PSCs show specific cellular dynamics, such as a short G1 phase and silenced cell-cycle checkpoints for high cellular proliferation. However, how exogenous DNA damage affects cell cycle-dependent centrosome number regulation in PSCs remains unknown. This study used human iPSCs (hiPSCs) derived from primary skin fibroblasts as a PSC model to address this question. hiPSCs derived from somatic cells could be a useful tool for addressing the radiation response in cell lineage differentiation. After radiation exposure, the hiPSCs showed a higher frequency of centrosome overduplication and multipolar cell division than the differentiated cells. To suppress the indirect effect of radiation exposure, we used the radical scavenger dimethyl sulfoxide (DMSO). Combined treatment with radiation and DMSO efficiently suppressed DNA damage and centrosome overduplication in hiPSCs. Our results will contribute to the understanding of the dynamics of stem cells and the assessment of the risk of genome instability for regenerative medicine.

    DOI: 10.1667/RADE-24-00069.1

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  • Structural study of wild-type and phospho-mimic XRCC4 dimer and multimer proteins using circular dichroism spectroscopy. International journal

    Kai Nishikubo, Maho Hasegawa, Yudai Izumi, Kentaro Fujii, Koichi Matsuo, Yoshihisa Matsumoto, Akinari Yokoya

    International journal of radiation biology   1 - 36   2023.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    PURPOSE: To investigate the structural features of wild-type and phospho-mimicking mutated XRCC4 protein, a protein involved in DNA double-strand break repair. MATERIALS AND METHODS: XRCC4 with a HisTag were expressed by E. coli harboring plasmid DNA and purified. Phospho-mimicking mutants in which one phosphorylation site was replaced with aspartic acid were also prepared in order to reproduce the negative charge resulting from phosphorylation. The proteins were separated into dimers and multimers by gel filtration chromatography. Circular dichroism (CD) spectroscopy was performed in the region from ultraviolet to vacuum-ultraviolet. The CD spectra were analyzed with two analysis programs to evaluate the secondary structures of the wild-type and phospho-mimicked dimers and multimers. RESULT AND DISCUSSION: The proportion of β-strand in the wild-type dimers was very low, particularly in their C-terminal region, including the five phosphorylation sites. The secondary structure of the phospho-mimic hardly changed from the monomeric to dimeric forms. In contrast, the β-strand content increased and the α-helix content decreased upon multimerization of the wild-type protein. The structural change of multimers slightly depended on the phospho-mimic site. These results suggest that the β-strand structure stabilizes the multimerization of XRCC4 and it is regulated by phosphorylation at the C-terminal site in living cells. CONCLUSION: An increase in the β-strand content in XRCC4 is essential for stabilization of the multimeric form through C-terminal phosphorylation, allowing formation of the large double-strand break repair machinery.

    DOI: 10.1080/09553002.2023.2214210

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  • APTX acts in DNA double-strand break repair in a manner distinct from XRCC4

    Rikiya Imamura, Mizuki Saito, Mikio Shimada, Junya Kobayashi, Masamichi Ishiai, Yoshihisa Matsumoto

    Journal of Radiation Research   64 ( 3 )   485 - 495   2023.3

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    Authorship:Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    Abstract

    Aprataxin (APTX), the product of the causative gene for hereditary neurogenerative syndromes Ataxia-oculomotor apraxia 1 and early onset ataxia with oculomotor apraxia and hypoalbuminemia, has an enzymatic activity of removing adenosine monophosphate from DNA 5′-end, which arises from abortive ligation by DNA ligases. It is also reported that APTX physically binds to XRCC1 and XRCC4, suggesting its involvement in DNA single-strand break repair (SSBR) and DNA double-strand break repair (DSBR) via non-homologous end joining pathway. Although the involvement of APTX in SSBR in association with XRCC1 has been established, the significance of APTX in DSBR and its interaction with XRCC4 have remained unclear. Here, we generated APTX knock-out (APTX−/−) cell from human osteosarcoma U2OS through CRISPR/Cas9-mediated genome editing system. APTX−/− cells exhibited increased sensitivity toward ionizing radiation (IR) and Camptothecin in association with retarded DSBR, as shown by increased number of retained γH2AX foci. However, the number of retained 53BP1 foci in APTX−/− cell was not discernibly different from wild-type cells, in stark contrast to XRCC4-depleted cells. The recruitment of GFP-tagged APTX (GFP-APTX) to the DNA damage sites was examined by laser micro-irradiation and live-cell imaging analysis using confocal microscope. The accumulation of GFP-APTX on the laser track was attenuated by siRNA-mediated depletion of XRCC1, but not XRCC4. Moreover, the deprivation of APTX and XRCC4 displayed additive inhibitory effects on DSBR after IR exposure and end joining of GFP reporter. These findings collectively suggest that APTX acts in DSBR in a manner distinct from XRCC4.

    DOI: 10.1093/jrr/rrad007

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  • Implication of E3 ligase RAD18 in UV-induced mutagenesis in human induced pluripotent stem cells and neuronal progenitor cells. International journal

    Mikio Shimada, Takumi Tokumiya, Tomoko Miyake, Kaima Tsukada, Norie Kanzaki, Hiromi Yanagihara, Junya Kobayashi, Yoshihisa Matsumoto

    Journal of radiation research   2023.1

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    Language:English   Publishing type:Research paper (scientific journal)  

    Pluripotent stem cells (PSCs) have the potential to differentiate to any of the other organs. The genome DNA integrity of PSCs is maintained by a high level of transcription for a number of genes involved in DNA repair, cell cycle and apoptosis. However, it remains unclear how high the frequency of genetic mutation is and how these DNA repair factors function in PSCs. In this study, we employed Sup F assay for the measurement of mutation frequency after UV-C irradiation in induced pluripotent stem cells (iPSCs) as PSC models and neural progenitor cells (NPCs) were derived from iPSCs as differentiated cells. iPSCs and NPCs exhibited a lower mutation frequency compared with the original skin fibroblasts. In RNA-seq analysis, iPSCs and NPCs showed a high expression of RAD18, which is involved in trans-lesion synthesis (TLS) for the emergency tolerance system during the replication process of DNA. Although RAD18 is involved in both error free and error prone TLS in somatic cells, it still remains unknown the function of RAD18 in PSCs. In this study we depleted of the RAD18 by siRNA knockdown resulted in decreased frequency of mutation in iPSCs and NPCs. Our results will provide information on the genome maintenance machinery in PSCs.

    DOI: 10.1093/jrr/rrac099

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  • THE ROLE OF DNA DOUBLE-STRAND BREAK REPAIR THROUGH NON-HOMOLOGOUS END JOINING IN THE DOSE-RATE EFFECT IN TERMS OF CLONOGENIC ABILITY

    Hisayo Tsuchiya, Mikio Shimada, Kaima Tsukada, Qingmei Meng, Junya Kobayashi, Yoshihisa Matsumoto

    Radiation Protection Dosimetry   198 ( 13-15 )   990 - 997   2022.9

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    Authorship:Last author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    Abstract

    It is generally and widely accepted that the biological effects of a given dose of ionizing radiation, especially those of low linear energy transfer radiations like X-ray and gamma ray, become smaller as the dose rate becomes lower. This phenomenon, known as ‘dose-rate effect (DRE),’ is considered due to the repair of sublethal damage during irradiation but the precise mechanisms for DRE have remained to be clarified. We recently showed that DRE in terms of clonogenic cell survival is diminished or even inversed in rodent cells lacking Ku, which is one of the essential factors in the repair of DNA double-strand breaks (DSBs) through non-homologous end joining (NHEJ). Here we review and discuss the involvement of NHEJ in DRE, which has potential implications in radiological protection and cancer therapeutics.

    DOI: 10.1093/rpd/ncac030

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  • 〈各論〉(1)中性子線によるDNA損傷とその修復の分子機構

    松本, 義久, 島田, 幹男, 今道, 祥二, 山西, 弘城, 松田, 外志朗

    近畿大学原子炉利用共同研究等経過報告書 令和2年度 = Annual Report of Cooperative Researches at Kindai University Reactor, 2020   89 - 91   2021.12

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:大阪大学大学院工学研究科  

    type:Journal Article
    3. 生物の放射線影響に関する研究(生物系)

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  • Prediction of treatment response from the microenvironment of tumor immunity in cervical cancer patients treated with chemoradiotherapy.

    Masanori Someya, Takaaki Tsuchiya, Yuki Fukushima, Tomokazu Hasegawa, Masakazu Hori, Mio Kitagawa, Toshio Gocho, Shoh Mafune, Yutaro Ikeuchi, Yoshihiko Hirohashi, Toshihiko Torigoe, Masahiro Iwasaki, Motoki Matsuura, Tsuyoshi Saito, Yoshihisa Matsumoto, Koh-Ichi Sakata

    Medical molecular morphology   54 ( 3 )   245 - 252   2021.9

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    To supplement clinical decision-making in the management of cervical cancer, various prognostic factors, including tumor immune microenvironments, were examined in patients with cervical cancer treated with definitive chemoradiotherapy. We retrospectively analyzed the expression of CD8, FoxP3, HLA-1, PD-L1, and XRCC4 in 100 cases of cervical cancer. The observed tumor immune microenvironments were also classified into three types: inflamed, excluded, and cold type. Less FoxP3+ T cells and cold-type tumor were found to be poor prognostic factors in addition to non-SCC, large pre-treatment tumor volume, and three or less cycles of concurrent chemotherapy based on multivariate analysis. Cold-type tumors had significantly worse prognoses than the other two types, whereas inflamed- and excluded-type tumors showed similar 5-year disease-specific survival (P < 0.001; 0% vs. 60.3% vs. 72.3%). Radiotherapy could overcome the inhibitory immune microenvironment that occurs in excluded type. Individualized combination therapy adapted to pre-treatment tumor immunity may be necessary to improve radiotherapy outcomes in cervical cancer.

    DOI: 10.1007/s00795-021-00290-w

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  • α-glucosyl-rutin activates immediate early genes in human induced pluripotent stem cells. International journal

    Tomoko Miyake, Munekazu Kuge, Yoshihisa Matsumoto, Mikio Shimada

    Stem cell research   56   102511 - 102511   2021.8

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    Rutin is a natural flavonoid glycoside found in several vegetables and fruits such as buckwheat and onion. Rutin has a range of pharmacological effects that include anti-oxidant, anti-inflammation, anti-bacterial, and anti-cancer activities. α-glucosyl-rutin (AGR) is a derivative of rutin with increased water solubility that is used in cosmetics and foods. However, the effects of AGR on cellular responses have not been clarified, especially in stem cells. Induced pluripotent stem cells (iPSCs) show high proliferative activity and pluripotency; however, regulation of molecular machinery such as cell cycle, metabolism, and DNA repair differs between iPSCs and somatic cells. Here, we compared the effects of AGR on iPSCs and differentiated cells (fibroblasts and skin keratinocytes). AGR-treated iPSCs exhibited increased cell viability. RNA sequencing and reverse transcriptase PCR analysis revealed that AGR induced expression of immediate early genes (IEGs) and differentiation-related genes in iPSCs. Our results suggest that AGR may activate differentiation signals mediated by IEG responses in iPSCs, resulting in altered metabolic activity and increased cell viability.

    DOI: 10.1016/j.scr.2021.102511

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  • Phosphorylation of PNKP mediated by CDKs promotes end-processing of Okazaki fragments during DNA replication

    Kaima Tsukada, Rikiya Imamura, Kotaro Saikawa, Mizuki Saito, Naoya Kase, Tomoko Miyake, Masamichi Ishiai, Yoshihisa Matsumoto, Mikio Shimada

    2021.7

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    Publisher:Cold Spring Harbor Laboratory  

    <title>Abstract</title>Polynucleotide kinase phosphatase (PNKP) has enzymatic activities as 3′ phosphatase and 5′ kinase of DNA ends to promote DNA ligation. Here, we show that PNKP is involved in progression of DNA replication through end-processing of Okazaki fragments (OFs). Cyclin-dependent kinases (CDKs) regulate phosphorylation on threonine 118 (T118) of PNKP, and which phosphorylation allows it to be recruited to OFs. Loss of PNKP and T118 phosphorylation significantly increased unligated OFs and high-speed DNA synthesis in replication forks, suggesting that PNKP T118 phosphorylation is required for OFs ligation for its maturation. Furthermore, phosphatase-dead PNKP also exhibited an accumulation of unligated OFs and high-speed DNA synthesis. Overall, our data suggested that CDK-mediated PNKP phosphorylation at T118 is important for its recruitment to OFs and PNKP subsequently promotes end-processing for OFs maturation for stable cell proliferation.

    DOI: 10.1101/2021.07.29.452278

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  • DNA-Dependent Protein Kinase Catalytic Subunit: The Sensor for DNA Double-Strand Breaks Structurally and Functionally Related to Ataxia Telangiectasia Mutated. International journal

    Yoshihisa Matsumoto, Anie Day D C Asa, Chaity Modak, Mikio Shimada

    Genes   12 ( 8 )   2021.7

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    The DNA-dependent protein kinase (DNA-PK) is composed of a DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and Ku70/Ku80 heterodimer. DNA-PK is thought to act as the "sensor" for DNA double-stranded breaks (DSB), which are considered the most deleterious type of DNA damage. In particular, DNA-PKcs and Ku are shown to be essential for DSB repair through nonhomologous end joining (NHEJ). The phenotypes of animals and human individuals with defective DNA-PKcs or Ku functions indicate their essential roles in these developments, especially in neuronal and immune systems. DNA-PKcs are structurally related to Ataxia-telangiectasia mutated (ATM), which is also implicated in the cellular responses to DSBs. DNA-PKcs and ATM constitute the phosphatidylinositol 3-kinase-like kinases (PIKKs) family with several other molecules. Here, we review the accumulated knowledge on the functions of DNA-PKcs, mainly based on the phenotypes of DNA-PKcs-deficient cells in animals and human individuals, and also discuss its relationship with ATM in the maintenance of genomic stability.

    DOI: 10.3390/genes12081143

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  • Functional analysis of XRCC4 mutations in reported microcephaly and growth defect patients in terms of radiosensitivity

    Anie Day D C Asa, Rujira Wanotayan, Mukesh Kumar Sharma, Kaima Tsukada, Mikio Shimada, Yoshihisa Matsumoto

    Journal of Radiation Research   2021.4

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    Authorship:Last author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    <title>Abstract</title>
    Non-homologous end joining is one of the main pathways for DNA double-strand break (DSB) repair and is also implicated in V(D)J recombination in immune system. Therefore, mutations in non-homologous end-joining (NHEJ) proteins were found to be associated with immunodeficiency in human as well as in model animals. Several human patients with mutations in XRCC4 were reported to exhibit microcephaly and growth defects, but unexpectedly showed normal immune function. Here, to evaluate the functionality of these disease-associated mutations of XRCC4 in terms of radiosensitivity, we generated stable transfectants expressing these mutants in XRCC4-deficient murine M10 cells and measured their radiosensitivity by colony formation assay. V83_S105del, R225X and D254Mfs*68 were expressed at a similar level to wild-type XRCC4, while W43R, R161Q and R275X were expressed at even higher level than wild-type XRCC4. The expression levels of DNA ligase IV in the transfectants with these mutants were comparable to that in the wild-type XRCC4 transfectant. The V83S_S105del transfectant and, to a lesser extent, D254Mfs*68 transfectant, showed substantially increased radiosensitivity compared to the wild-type XRCC4 transfectant. The W43R, R161Q, R225X and R275X transfectants showed a slight but statistically significant increase in radiosensitivity compared to the wild-type XRCC4 transfectant. When expressed as fusion proteins with Green fluorescent protein (GFP), R225X, R275X and D254Mfs*68 localized to the cytoplasm, whereas other mutants localized to the nucleus. These results collectively indicated that the defects of XRCC4 in patients might be mainly due to insufficiency in protein quantity and impaired functionality, underscoring the importance of XRCC4’s DSB repair function in normal development.

    DOI: 10.1093/jrr/rrab016

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  • Diminished or inversed dose-rate effect on clonogenic ability in Ku-deficient rodent cells International journal

    Hisayo Tsuchiya, Mikio Shimada, Kaima Tsukada, Qingmei Meng, Junya Kobayashi, Yoshihisa Matsumoto

    Journal of Radiation Research   62 ( 2 )   198 - 205   2020.12

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    <title>Abstract</title>
    The biological effects of ionizing radiation, especially those of sparsely ionizing radiations like X-ray and γ-ray, are generally reduced as the dose rate is reduced. This phenomenon is known as ‘the dose-rate effect’. The dose-rate effect is considered to be due to the repair of DNA damage during irradiation but the precise mechanisms for the dose-rate effect remain to be clarified. Ku70, Ku86 and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) are thought to comprise the sensor for DNA double-strand break (DSB) repair through non-homologous end joining (NHEJ). In this study, we measured the clonogenic ability of Ku70-, Ku86- or DNA-PKcs-deficient rodent cells, in parallel with respective control cells, in response to high dose-rate (HDR) and low dose-rate (LDR) γ-ray radiation (~0.9 and ~1 mGy/min, respectively). Control cells and murine embryonic fibroblasts (MEF) from a severe combined immunodeficiency (scid) mouse, which is DNA-PKcs-deficient, showed higher cell survival after LDR irradiation than after HDR irradiation at the same dose. On the other hand, MEF from Ku70−/− mice exhibited lower clonogenic cell survival after LDR irradiation than after HDR irradiation. XR-V15B and xrs-5 cells, which are Ku86-deficient, exhibited mostly identical clonogenic cell survival after LDR and HDR irradiation. Thus, the dose-rate effect in terms of clonogenic cell survival is diminished or even inversed in Ku-deficient rodent cells. These observations indicate the involvement of Ku in the dose-rate effect.

    DOI: 10.1093/jrr/rraa128

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  • DNA‑Dependent Protein Kinase in DNA Damage Response: Three Decades and Beyond Invited Reviewed

    Yoshihisa Matsumoto, Mukesh Kumar Sharma

    Journal of Radiation and Cancer Research   2020.12

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

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  • 〈各論〉(1)中性子線によるDNA 損傷とその修復の分子機構

    松本, 義久, 島田, 幹男, 今道, 祥二, 山西, 弘城, 松田, 外志朗

    近畿大学原子炉等利用共同研究経過報告書 平成31(令和元)年度 = Annual Report of Cooperative Researches at Kindai University Reactor, 2019   111 - 113   2020.12

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:大阪大学大学院工学研究科  

    type:Journal Article

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  • The FHA domain of PNKP is essential for its recruitment to DNA damage sites and maintenance of genome stability

    Kaima Tsukada, Mikio Shimada, Rikiya Imamura, Kotaro Saikawa, Masamichi Ishiai, Yoshihisa Matsumoto

    Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis   822   111727 - 111727   2020.11

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    Authorship:Last author   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.mrfmmm.2020.111727

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  • DNA修復タンパク質XRCC4多量体のリン酸化による構造変化(Structural changes of DNA repair protein XRCC4 due to phosphorylation and its role for multimerization)

    西久保 開, 長谷川 真保, 泉 雄大, 藤井 健太郎, 松尾 光一, 松本 義久, 横谷 明徳

    日本放射線影響学会大会講演要旨集   63回   76 - 76   2020.10

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    Language:English   Publisher:(一社)日本放射線影響学会  

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  • Linker region is required for efficient nuclear localization of polynucleotide kinase phosphatase

    Kaima Tsukada, Yoshihisa Matsumoto, Mikio Shimada

    PLOS ONE   15 ( 9 )   e0239404 - e0239404   2020.9

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    Publishing type:Research paper (scientific journal)   Publisher:Public Library of Science (PLoS)  

    DOI: 10.1371/journal.pone.0239404

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  • Differential expression of DNA-dependent protein kinase catalytic subunit in the brain of neonatal mice and young adult mice

    Aoi OKAWA, Takamitsu MORIOKA, Tatsuhiko IMAOKA, Shizuko KAKINUMA, Yoshihisa MATSUMOTO

    Proceedings of the Japan Academy, Series B   96 ( 5 )   171 - 179   2020.5

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  • Prediction of Results of Radiotherapy With Ku70 Expression and an Artificial Neural Network

    TOMOKAZU HASEGAWA, MASANORI SOMEYA, MASAKAZU HORI, TAKAAKI TSUCHIYA, YUUKI FUKUSHIMA, YOSHIHISA MATSUMOTO, KOH-ICHI SAKATA

    In Vivo   34 ( 5 )   2865 - 2872   2020

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    DOI: 10.21873/invivo.12114

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  • Reprogramming and differentiation-dependent transcriptional alteration of DNA damage response and apoptosis genes in human induced pluripotent stem cells Reviewed

    Shimada M, Tsukada K, Kagawa N, Matsumoto Y

    Journal of Radiation Research   60 ( 6 )   719 - 728   2019.11

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    DOI: 10.1093/jrr/rrz057

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  • DNA Damage Response After Ionizing Radiation Exposure in Skin Keratinocytes Derived from Human-Induced Pluripotent Stem Cells Reviewed

    Tomoko Miyake, M. Shimada, Yoshihisa Matsumoto, Akitoshi Okino

    International Journal of Radiation Oncology Biology Physics   105 ( 1 )   193 - 205   2019.9

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    DOI: 10.1016/j.ijrobp.2019.05.006

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  • DOSE-RATE and CELL-KILLING SENSITIVITY of HIGH-LINEAR ENERGY TRANSFER ION BEAM Reviewed

    Y. Furusawa, Y. Matsumoto, R. Hirayama, D. Ohsawa, T. Konishi

    Radiation Protection Dosimetry   183 ( 1-2 )   219 - 222   2019.5

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  • Influence of XRCC4 expression by breast cancer cells on ipsilateral recurrence after breast-conserving therapy Reviewed International journal

    Kitagawa M, Someya M, Hasegawa T, Mikami T, Asaishi K, Hasegawa T, Matsumoto Y, Kutomi G, Takemasa I, Sakata K

    Strahlentherapie und Oncologie   195 ( 7 )   648 - 658   2019.4

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    BACKGROUND: We examined the expression of nonhomologous end-joining (NHEJ) proteins by breast cancer cells in patients with or without ipsilateral breast tumor recurrence (IBTR) after breast-conserving therapy. We also investigated whether there was a difference of NHEJ-related protein expression by tumor cells between two types of IBTR, i.e., true recurrence (TR) with regrowth from the tumor bed or development of a new primary tumor (NP). PATIENTS AND METHODS: The original cohort comprised 560 breast cancer patients who received breast-conserving therapy between February 1995 and March 2006, including 520 patients without IBTR and 40 patients with IBTR. Propensity score matching was employed to select 40 trios (120 patients) consisting of 1 patient with IBTR and 2 patients without IBTR. Immunohistochemical examination of proteins related to NHEJ was performed in surgical specimens. RESULTS: The 40 patients with IBTR included 22 patients who developed TR and 18 who had NP. The 15-year overall survival rate was 85.9% for patients with NP and 95.5% for those with TR, while it was 96.5% for patients without IBTR. Patients with high XRCC4 expression in tumor cells had significantly higher IBTR rates than those with low XRCC4 expression (P < 0.001). The frequency of TR was significantly higher in patients with high expression of XRCC4 than in those with low XRCC4 expression (p < 0.001). XRCC4 expression by tumor cells was not significantly related to development of NP. CONCLUSION: IBTR due to TR may be related to low radiosensitivity of tumor cells, possibly related to high XRCC4 expression.

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  • 〈各論〉(4) 中性子線によるDNA 損傷とその修復の分子機構

    松本, 義久, 島田, 幹男, 山西, 弘城, 松田, 外志朗, 今道, 祥二

    近畿大学原子炉等利用共同研究経過報告書 平成29年度 = Annual Report of Cooperative Researches at Kindai University Reactor, 2017   81 - 83   2018.12

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  • Structural analysis of DNA repair protein XRCC4 applying circular dichroism in an aqueous solution Reviewed

    Nishikubo K, Izumi Y, Matsumoto Y, Fujii K, Matsuo K, Yokoya A

    Radiation Protection Dosimetry.   183 ( 1-2 )   36 - 39   2018.10

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    DOI: 10.1093/rpd/ncy275

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  • In cellulo phosphorylation of DNA double-strand break repair protein XRCC4 on Ser260 by DNA-PK Reviewed

    Amiri Moghani AR, Sharma MK, Matsumoto Y

    Journal of Radiation Research.   59 ( 6 )   700 - 708   2018.9

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    DOI: 10.1093/jrr/rry072

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  • Caspase-mediated cleavage of X-ray repair cross-complementing group 4 promotes apoptosis by enhancing nuclear translocation of caspase-activated DNase Reviewed International journal

    Yumi Sunatani, Radhika Pankaj Kamdar, Mukesh Kumar Sharma, Tadashi Matsui, Ryo Sakasai, Mitsumasa Hashimoto, Yasuhito Ishigaki, Yoshihisa Matsumoto, Kuniyoshi Iwabuchi

    Experimental Cell Research.   362 ( 2 )   450 - 460   2017.12

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    X-ray repair cross-complementing group 4 (XRCC4), a repair protein for DNA double-strand breaks, is cleaved by caspases during apoptosis. In this study, we examined the role of XRCC4 in apoptosis. Cell lines, derived from XRCC4-deficient M10 mouse lymphoma cells and stably expressing wild-type XRCC4 or caspase-resistant XRCC4, were established and treated with staurosporine (STS) to induce apoptosis. In STS-induced apoptosis, expression of wild-type, but not caspase-resistant, XRCC4 in XRCC4-deficient cells enhanced oligonucleosomal DNA fragmentation and the appearance of TUNEL-positive cells by promoting nuclear translocation of caspase-activated DNase (CAD), a major nuclease for oligonucleosomal DNA fragmentation. CAD activity is reportedly regulated by the ratio of two inhibitor of CAD (ICAD) splice variants, ICAD-L and ICAD-S mRNA, which, respectively, produce proteins with and without the ability to transport CAD into the nucleus. The XRCC4-dependent promotion of nuclear import of CAD in STS-treated cells was associated with reduction of ICAD-S mRNA and protein, and enhancement of phosphorylation and nuclear import of serine/arginine-rich splicing factor (SRSF) 1. These XRCC4-dependent, apoptosis-enhancing effects were canceled by depletion of SRSF1 or SR protein kinase (SRPK) 1. In addition, overexpression of SRSF1 in XRCC4-deficient cells restored the normal level of apoptosis, suggesting that SRSF1 functions downstream of XRCC4 in activating CAD. This XRCC4-dependent, SRPK1/SRSF1-mediated regulatory mechanism was conserved in apoptosis in Jurkat human leukemia cells triggered by STS, and by two widely used anti-cancer agents, Paclitaxel and Vincristine. These data imply that the level of XRCC4 expression could be used to predict the effects of apoptosis-inducing drugs in cancer treatment.

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  • Pushing the haystack aside for efficient gene targeting in human cells Reviewed

    Yoshihisa Matsumoto

    FEBS JOURNAL   284 ( 17 )   2745 - 2747   2017.9

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    DOI: 10.1111/febs.14164

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  • Medicinally important aromatic plants with radioprotective activity Reviewed

    Samartha RM, Samartha M, Matsumoto Y

    Future Science OA   3 ( 4 )   FSO247   2017.4

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  • Influence of XRCC4 expression in esophageal cancer cells on the response to radiotherapy Reviewed

    Masakazu Hori, Masanori Someya, Yoshihisa Matsumoto, Kensei Nakata, Mio Kitagawa, Tomokazu Hasegawa, Takaaki Tsuchiya, Yuki Fukushima, Toshio Gocho, Yasushi Sato, Hiroyuki Ohnuma, Junji Kato, Shintaro Sugita, Tadashi Hasegawa, Koh-Ichi Sakata

    MEDICAL MOLECULAR MORPHOLOGY   50 ( 1 )   25 - 33   2017.3

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  • Expression of Ku70 predicts results of radiotherapy in prostate cancer Reviewed

    Tomokazu Hasegawa, Masanori Someya, Masakazu Hori, Yoshihisa Matsumoto, Kensei Nakata, Masanori Nojima, Mio Kitagawa, Takaaki Tsuchiya, Naoya Masumori, Tadashi Hasegawa, Koh-ichi Sakata

    STRAHLENTHERAPIE UND ONKOLOGIE   193 ( 1 )   29 - 37   2017.1

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  • A Live Cell DNA Damage Response Indicator System Based On p53 Regulation Mechanism

    Tsukada Kaima, Shimada Mikio, Matsumoto Yoshihisa

    Transactions of Japanese Society for Medical and Biological Engineering   55 ( 5 )   453 - 453   2017

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    <p>p53 is one of the most essential tumor suppressor and its abundance is tightly regulated in cells: in normal state, the amount of p53 is kept low through ubiquitylation by MDM2 and subsequent degradation by proteasome. In response to DNA damage, p53 undergoes phosphorylation by ATM, which interferes with its association with MDM2, and, as the result, its abundance is greatly increased. We sought to develop a live cell imaging system to monitor the cellular status of DNA damage response based on this life cycle of p53. We first introduced a plasmid vector (pEGFP-C1) expressing GFP-p53 fusion protein into human cancer cells with normal p53, mutant p53 and p53 deletion and analyzed p53 abundance and its change after irradiation by Western blotting and flowcytometry. Furthermore, we are in progress to engineer cells to express p53-GFP fusion gene from chromosome by CRISPR/Cas9 genome editing technology.</p>

    DOI: 10.11239/jsmbe.55Annual.453

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  • Effect of different dose rates of ionizing radiation on ciliogenesis in hTERT-RPE1 cells Reviewed

    Mikio Shimada, Hisayo Tsuchiya, Yoshihisa Matsumoto

    Energy Procedia   131   444 - 447   2017

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    DOI: 10.1016/j.egypro.2017.09.425

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  • Local tumor control and DNA-PK activity of peripheral blood lymphocytes in prostate cancer patients receiving radiotherapy Reviewed

    Someya, Masanori, Hasegawa, Tomokazu, Hori, Masakazu, Matsumoto, Yoshihisa, Nakata, Kensei, Masumori, Naoya, Sakata, Koh-ichi

    Journal of Radiation Research   58 ( 2 )   225 - 231   2017

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  • LIG4 mediates Wnt signalling-induced radioresistance Reviewed

    Sohee Jun, Youn-Sang Jung, Han Na Suh, Wenqi Wang, Moon Jong Kim, Young Sun Oh, Esther M. Lien, Xi Shen, Yoshihisa Matsumoto, Pierre D. McCrea, Lei Li, Junjie Chen, Jae-Il Park

    NATURE COMMUNICATIONS   7   10994   2016.3

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    DOI: 10.1038/ncomms10994

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  • Influence of Ku86 and XRCC4 expression in uterine cervical cancer on the response to preoperative radiotherapy Reviewed

    Takada Y, Someya M, Matsumoto Y, Satoh M, Nakata K, Hori M, Saito M, Horikawa N, Tateoka K, Teramoto M, Saito T, Hasegawa T, Sakata K

    Medical Molecular Morphology.   49 ( 4 )   210 - 216   2016.2

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  • In cellulo phosphorylation of XRCC4 Ser320 by DNA-PK induced by DNA damage Reviewed

    Sharma, Mukesh Kumar, Imamichi, Shoji, Fukuchi, Mikoto, Samarth, Ravindra Mahadeo, Tomita, Masanori, Matsumoto, Yoshihisa

    Journal of Radiation Research   57 ( 2 )   115 - 120   2016

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  • DNA-PKcs Is Involved in Ig Class Switch Recombination in Human B Cells Reviewed

    Andrea Bjorkman, Likun Du, Kerstin Felgentreff, Cornelia Rosner, Radhika Pankaj Kamdar, Georgia Kokaraki, Yoshihisa Matsumoto, E. Graham Davies, Mirjam van der Burg, Luigi D. Notarangelo, Lennart Hammarstrom, Qiang Pan-Hammarstrom

    JOURNAL OF IMMUNOLOGY   195 ( 12 )   5608 - 5615   2015.12

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  • Lysine 271 but not lysine 210 of XRCC4 is required for the nuclear localization of XRCC4 and DNA ligase IV Reviewed

    Mikoto Fukuchi, Rujira Wanotayan, Sicheng Liu, Shoji Imamichi, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   461 ( 4 )   687 - 694   2015.6

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  • Asparagine 326 in the extremely C-terminal region of XRCC4 is essential for the cell survival after irradiation Reviewed

    Rujira Wanotayan, Mikoto Fukuchi, Shoji Imamichi, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   457 ( 4 )   526 - 531   2015.2

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  • Recognition and Repair of DNA Double-strand Breaks – From Molecular Biology to Cancer Diagnosis and Therapeutics-

    Matsumoto Yoshihisa

    Proceedings of the 334d Symposium on Materials Science and Engineering Research Center of Ion Beam Technology Hosei University   1 - 10   2015.1

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  • Ionizing radiation-induced XRCC4 phosphorylation is mediated through ATM in addition to DNA-PK. Reviewed

    Shoji Imamichi, Mukesh Kumar Sharma, Radhika Pankaj Kamdar, Mikoto Fukuchi, Yoshihisa Matsumoto

    Proceedings of the Japan Academy. Series B, Physical and biological sciences   90 ( 9 )   365 - 72   2014

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    XRCC4 (X-ray cross-complementation group 4) is a protein associated with DNA ligase IV, which is thought to join two DNA ends at the final step of DNA double-strand break repair through non-homologous end-joining. It has been shown that, in response to irradiation or treatment with DNA damaging agents, XRCC4 undergoes phosphorylation, requiring DNA-PK. Here we explored possible role of ATM, which is structurally related to DNA-PK, in the regulation of XRCC4. The radiosensitizing effects of DNA-PK inhibitor and/or ATM inhibitor were dependent on XRCC4. DNA-PK inhibitor and ATM inhibitor did not affect the ionizing radiation-induced chromatin recruitment of XRCC4. Ionizing radiation-induced phosphorylation of XRCC4 in the chromatin-bound fraction was largely inhibited by DNA-PK inhibitor but further diminished by the combination with ATM inhibitor. The present results indicated that XRCC4 phosphorylation is mediated through ATM as well as DNA-PK, although DNA-PK plays the major role. We would propose a possible model that DNA-PK and ATM acts in parallel upstream of XRCC4, regulating through phosphorylation.

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  • Smart Choice between Two DNA Double-strand Break Repair Mechanisms

    Matsumoto Yoshihisa

    Japanese Journal of Medical Physics   34 ( 2 )   57 - 64   2014

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    DNA double-strand break (DSB) is considered most deleterious among radiation-induced DNA damages and most relevant to the biological effects of radiation. In eukaryotic cells, DSB is repaired mainly through two pathways: non-homologous end-joining (NHEJ) and homologous recombination (HR). These repair pathways seem to play complementary roles. NHEJ is considered less accurate than HR, but HR is available only in late S and G2 phases in vertebrates. Recent studies elucidated how cells choose one from these two pathways depending on the circumstance: cell cycle phase, complexity of DNA damage and chromatin structure.

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  • Ionizing radiation-induced XRCC4 phosphorylation is mediated through ATM in addition to DNA-PK Reviewed

    Imamichi, Shoji, Sharma, Mukesh Kumar, Kamdar, Radhika Pankaj, Fukuchi, Mikoto, Matsumoto, Yoshihisa

    Proceedings of the Japan Academy Series B-Physical and Biological Sciences   90 ( 9 )   365 - 372   2014

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  • Function of XRCC4 C-terminal region in DNA double-strand break repair

    Rujira Wanotayan, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    Transactions of the American Nuclear Society   111   1145 - 1148   2014

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  • C-terminal region of DNA ligase IV drives XRCC4/DNA ligase IV complex to chromatin Reviewed

    Sicheng Liu, Xunyue Liu, Radhika Pankaj Kamdar, Rujira Wanotayan, Mukesh Kumar Sharma, Noritaka Adachi, Yoshihisa Matsumoto

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   439 ( 2 )   173 - 178   2013.9

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  • Analysis and results of Ku and XRCC4 expression in hypopharyngeal cancer tissues treated with chemoradiotherapy Reviewed

    Jyunichi Hayashi, Koh-Ichi Sakata, Masanori Someya, Yoshihisa Matsumo, Masaaki Satoh, Kensei Nakata, Masakazu Hori, Masaru Takagi, Atsushi Kondoh, Tetsuo Himi, Masato Hareyama

    ONCOLOGY LETTERS   4 ( 1 )   151 - 155   2012.7

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  • The combination of olaparib and camptothecin for effective radiosensitization Reviewed

    Katsutoshi Miura, Koh-ichi Sakata, Masanori Someya, Yoshihisa Matsumoto, Hideki Matsumoto, Akihisa Takahashi, Masato Hareyama

    RADIATION ONCOLOGY   7   62   2012.4

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  • The combination of hyperthermia or chemotherapy with gimeracil for effective radiosensitization Reviewed

    M. Takagi, K. Sakata, M. Someya, Y. Matsumoto, H. Tauchi, M. Hareyama, M. Fukushima

    STRAHLENTHERAPIE UND ONKOLOGIE   188 ( 3 )   255 - 261   2012.3

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  • Effects of Depletion of Dihydropyrimidine Dehydrogenase on Focus Formation and RPA Phosphorylation Reviewed

    Masanori Someya, Koh-ichi Sakata, Yoshihisa Matsumoto, Hiroshi Tauchi, Masahiro Kai, Masato Hareyama, Masakazu Fukushima

    JOURNAL OF RADIATION RESEARCH   53 ( 2 )   250 - 256   2012.3

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  • DNA-PK inhibition causes a low level of H2AX phosphorylation and homologous recombination repair in Medaka (Oryzias latipes) cells Reviewed

    Urushihara, Yusuke, Kobayashi, Junya, Matsumoto, Yoshihisa, Komatsu, Kenshi, Oda, Shoji, Mitani, Hiroshi

    Biochemical and Biophysical Research Communications   429 ( 3-4 )   131 - 136   2012

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  • Identification of DNA-Dependent Protein Kinase Catalytic Subunit (DNA-PKcs) as a Novel Target of Bisphenol A Reviewed

    Ito, Yuki, Ito, Takumi, Karasawa, Satoki, Enomoto, Teruya, Nashimoto, Akihiro, Hase, Yasuyoshi, Sakamoto, Satoshi, Mimori, Tsuneyo, Matsumoto, Yoshihisa, Yamaguchi, Yuki, Handa, Hiroshi

    Plos One   7 ( 12 )   e50481   2012

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  • Biological Defense Mechanisms against DNA Double-Strand Break and Their Possible Medical Applications

    MATSUMOTO Yoshihisa

    J. Surf. Sci. Soc. Jpn.   32 ( 9 )   569 - 574   2011.9

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    Radiation is now widely used for clinical diagnosis and therapeutics. On the other hand, radiation influences various tissues represented by immunological and reproductive systems, and is also recognized as one of the cause of carcinogenesis. Such pleiotropic effects of radiation are mediated through generation of damages on DNA molecule, vitally important genetic macromolecule. Among various types of DNA damages, double-strand break (DSB) is considered most critical and, therefore, responsible for biological effects. DSB is repaired mainly through two pathways: non-homologous end joining (NHEJ) and homologous recombination (HR). Understanding of these mechanisms has been greatly deepened in past 20 years and is now providing a promising approach toward cancer therapy. We have studied the mechanisms of NHEJ, focusing especially on the role of phosphorylation and the assembly of machinery therein, which will be introduced below.

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  • Gimeracil, an inhibitor of dihydropyrimidine dehydrogenase, inhibits the early step in homologous recombination Reviewed

    Koh-Ichi Sakata, Masanori Someya, Yoshihisa Matsumoto, Hiroshi Tauchi, Masahiro Kai, Minoru Toyota, Masaru Takagi, Masato Hareyama, Masakazu Fukushima

    CANCER SCIENCE   102 ( 9 )   1712 - 1716   2011.9

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  • 【基礎と臨床の対話】放射線増感剤の基礎と臨床 ギメラシルによる放射線増感作用

    坂田 耕一, 高木 克, 染谷 正則, 田内 広, 松本 義久, 晴山 雅人, 福島 正和

    癌の臨床   56 ( 6 )   441 - 443   2011.4

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  • The association of DNA-dependent protein kinase activity of peripheral blood lymphocytes with prognosis of cancer Reviewed

    Someya, M., Sakata, K-I, Matsumoto, Y., Kamdar, R. P., Kai, M., Toyota, M., Hareyama, M.

    British Journal of Cancer   104 ( 11 )   1724 - 1729   2011

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  • Gene Expression Associated with DNA-Dependent Protein Kinase Activity under Normoxia, Hypoxia, and Reoxygenation Reviewed

    Tsuchimoto, Tadashi, Sakata, Koh-ichi, Someya, Masanori, Yamamoto, Hiroyuki, Hirayama, Ryoichi, Matsumoto, Yoshihisa, Furusawa, Yoshiya, Hareyama, Masato

    Journal of Radiation Research   52 ( 4 )   464 - 471   2011

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  • Gimeracil sensitizes cells to radiation via inhibition of homologous recombination Reviewed

    Masaru Takagi, Koh-ichi Sakata, Masanori Someya, Hiroshi Tauchi, Kenta Iijima, Yoshihisa Matsumoto, Toshihiko Torigoe, Akari Takahashi, Masato Hareyama, Masakazu Fukushima

    RADIOTHERAPY AND ONCOLOGY   96 ( 2 )   259 - 266   2010.8

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  • Edaravone, a known free radical scavenger, enhances X-ray-induced apoptosis at low concentrations Reviewed

    N. Sasano, A. Enomoto, Y. Hosoi, Y. Katsumura, Y. Matsumoto, A. Morita, K. Shiraishi, K. Miyagawa, H. Igaki, K. Nakagawa

    CANCER LETTERS   293 ( 1 )   52 - 57   2010.7

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  • Sodium Orthovanadate Inhibits p53-Mediated Apoptosis Reviewed

    Akinori Morita, Shinichi Yamamoto, Bing Wang, Kaoru Tanaka, Norio Suzuki, Shin Aoki, Azusa Ito, Tomohisa Nanao, Soichiro Ohya, Minako Yoshino, Jin Zhu, Atsushi Enomoto, Yoshihisa Matsumoto, Osamu Funatsu, Yoshio Hosoi, Masahiko Ikekita

    CANCER RESEARCH   70 ( 1 )   257 - 265   2010.1

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  • Radiation-induced XRCC4 Association with Chromatin DNA Analyzed by Biochemical Fractionation Reviewed

    Kamdar, Radhika Pankaj, Matsumoto, Yoshihisa

    Journal of Radiation Research   51 ( 3 )   303 - 313   2010

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  • ギメラシルの放射線増感効果の検討

    高木 克, 坂田 耕一, 染谷 正則, 林 潤一, 小島 一男, 中田 健生, 晴山 雅人, 松本 義久, 田内 広, 福島 正和

    頭頸部癌   35 ( 2 )   179 - 179   2009.5

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  • Sodium orthovanadate is a bifunctional inhibitor of transcription-dependent and -independent p53-mediated apoptosis

    MORITA Akinori, YAMAMOTO Shinichi, WANG Bing, TANAKA Kaoru, SUZUKI Norio, AOKI Shin, ITO Azusa, NANAO Tomohisa, OHYA Soichiro, YOSHINO Minako, ENOMOTO Atsushi, MATSUMOTO Yoshihisa, FUNATSU Osamu, HOSOI Yoshio, IKEKITA Masahiko

    The Japan Radiation Research Society Annual Meeting Abstracts   2009   140 - 140   2009

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    We recently reported a novel suppressive effect of sodium orthovanadate (vanadate) on the DNA-binding activity of p53. In this study, we initially showed that vanadate had a more potent antiapoptotic activity than three other chemical p53 inhibitors, including pifithrin-α (PFTα), a well-known inhibitor of p53. Although the other agents inhibited the p53 transcriptional activity, they did not suppress p53-dependent apoptosis in irradiated MOLT-4 cells. Further investigations using cells with defective or impaired p53 function indicated vanadate’s specificity for p53 in suppressing DNA damage-induced apoptosis. To investigate the cause for the different effects of vanadate and the other inhibitors, we chose PFTα and PFTµ (an inhibitor of p53-mediated transcription-independent apoptotic pathway), as references, and determined the effect of them and vanadate on p53-mediated apoptosis, with a particular focus on the transcription-independent pathway. We found that vanadate suppressed the p53-associated apoptotic events at the mitochondria, such as the loss of the mitochondrial membrane potential, the conformational change of Bax and Bak, the mitochondrial translocation of p53, and its interaction with Bcl-2. Vanadate also suppressed the apoptosis-inducing activity of mitochondrially-targeted temperature-sensitive p53 in stable transfectants of the SaOS-2 cell line. Finally, we tested vanadate’s potential use as a radioprotector. Vanadate completely protected mice from a sublethal dose of 8 Gy and partially from a lethal dose of 12 Gy. Our data demonstrate that vanadate can suppress both the transcription-dependent and the transcription-independent pathways, and suggest that both pathways must be inhibited to completely block p53-mediated apoptosis.

    DOI: 10.11513/jrrsabst.2009.0.140.1

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  • Characterization of a cancer cell line that expresses a splicing variant form of 53BP1: Separation of checkpoint and repair functions in 53BP1 Reviewed

    Kuniyoshi Iwabuchi, Tadashi Matsui, Mitsumasa Hashimoto, Yoshihisa Matsumoto, Takayuki Kurihara, Takayasu Date

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   376 ( 3 )   509 - 513   2008.11

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    DOI: 10.1016/j.bbrc.2008.09.022

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  • Role of DNA Double-strand Break Repair Genes in Cell Proliferation under Low Dose-rate Irradiation Conditions Reviewed

    Masanori Tomita, Fumiko Morohoshi, Yoshihisa Matsumoto, Kensuke Otsuka, Kazuo Sakai

    JOURNAL OF RADIATION RESEARCH   49 ( 5 )   557 - 564   2008.9

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  • Negative regulation of MEKK1/2 signaling by Serine-Threonine kinase 38 (STK38) Reviewed

    A. Enomoto, N. Kido, M. Ito, A. Morita, Y. Matsumoto, N. Takamatsu, Y. Hosoi, K. Miyagawa

    ONCOGENE   27 ( 13 )   1930 - 1938   2008.3

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  • ギメラシルの放射線増感効果の分子メカニズム

    坂田 耕一, 染谷 正則, 高木 克, 中田 健生, 小島 一男, 晴山 雅人, 田内 広, 松本 義久, 福島 正和

    日本医学放射線学会学術集会抄録集   67回   S254 - S255   2008.2

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  • 分割照射や抗癌剤併用におけるギメラシルの放射線増感作用の検討

    高木 克, 坂田 耕一, 染谷 正則, 林 潤一, 小島 一男, 中田 健生, 晴山 雅人, 松本 義久, 田内 広, 福島 正和

    日本医学放射線学会学術集会抄録集   67回   S254 - S254   2008.2

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  • ギメラシルの放射線増感作用の放射線誘発γH2AXフォーカスによる解析

    染谷 正則, 高木 克, 小島 一男, 中田 健生, 坂田 耕一, 晴山 雅人, 田内 広, 松本 義久, 福島 正和

    日本医学放射線学会学術集会抄録集   67回   S254 - S254   2008.2

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  • Mechanism of inhibitory effect of sodium orthovanadate on transcription-independent p53-induced apoptosis

    MORITA Akinori, YAMAMOTO Shinichi, WANG Bing, TANAKA Kaoru, ITO Azusa, ENOMOTO Atsushi, MATSUMOTO Yoshihisa, FUNATSU Osamu, HOSOI Yoshio, SUZUKI Norio, IKEKITA Masahiko

    The Japan Radiation Research Society Annual Meeting Abstracts   2008   142 - 142   2008

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    We recently reported a novel suppressive effect of sodium orthovanadate (vanadate) on the DNA-binding activity of p53. In this study, we initially showed that vanadate had more potent antitapoptotic activity than other three chemical p53 inhibitors including pifithrin-alfa (PFT), a well-known inhibitor of p53. Although others inhibited the p53 transcriptional activity, they were not able to suppress p53-dependent apoptosis in irradiated MOLT-4 cells. To pursue the difference between the vanadate's effect and others, we chose PFT as a reference, and determined the effect of each inhibitor on p53-mediated apoptosis, especially focused on transcription-independent pathway. The following experiments revealed that vanadate showed more potent suppressive effect on p53-associated mitochondrial apoptotic events, such as the loss of mitochondrial membrane potential, the conformational change of Bax and Bak, the ubiquitilation and mitochondrial translocation of p53, and the interaction of p53 with Bcl-2. In addition, vanadate was capable of suppressing the apoptosis-inducing activity of mitochondrially targeted p53 in temperature-sensitive SaOS-2 stable transfectants. Our data demonstrate that vanadate can also suppress the transcription-independent pathway, and suggest the possibility that inhibition of both the transcription-dependent and transcription-independent pathways is needed to sufficient suppression of p53-mediated apoptosis.

    DOI: 10.11513/jrrsabst.2008.0.142.0

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  • 放射光X線マイクロビームによるDNA損傷に対する細胞の応答(Cellular response to DNA damage induced by synchrotron X-ray microbeam)

    冨田 雅典, 前田 宗利, 宇佐美 徳子, 松本 義久, 小林 克己

    生物物理   47 ( Suppl.1 )   S268 - S268   2007.11

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  • 乳癌患者におけるリンパ球DNA-PK活性、放射線誘発NBS1フォーカスと臨床的悪性度の関係

    染谷 正則, 坂田 耕一, 松本 義久, 晴山 雅人

    日本医学放射線学会学術集会抄録集   66回   S351 - S351   2007.2

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  • Free radical scavenger edaravone suppresses X-ray-induced apoptosis through p53 inhibition in MOLT-4 cells Reviewed

    Sasano, Nakashi, Enomot, Atsushi, Hos, Yoshio, Katsumura, Yosuke, Matsumo, Yoshihisa, Shiraishi, Kenshiro, Miyagawa, Kiyoshi, Igaki, Hiroshi, Nakagawa, Keiichi

    Journal of Radiation Research   48 ( 6 )   495 - 503   2007

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  • Mechanism of suppressive effect of sodium orthovanadate on p53

    YAMAMOTO Shinichi, MORITA Akinori, ITO Azusa, ENOMOTO Atsushi, MATSUMOTO Aoshihisa, FUNATSU Osamu, HOSOI Yoshio, SUZUKI Norio, IKEKITA Masahiko

    The Japan Radiation Research Society Annual Meeting Abstracts   2007   190 - 190   2007

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    The tumor suppressor p53 protects the cell against cancer by inducing apoptosis in response to multiple stresses. Some 50% of human cancers have mutations or deletions in the gene for p53 that inactivate or impair its apoptotic potential. On the other hand, in cancer therapy, p53 causes severe side effects by inducing excessive apoptotic death in several normal tissues. Thus, p53 inhibitory drugs have been suggested to rescue the acute response to cancer therapy. In this respect, recent studies have shown transcription-independent p53-mediated apoptosis via mitochondria. These findings indicate that effective p53 inhibitors should suppress both transcription-dependent and -independent pathways. We have reported a novel effect of sodium orthovanadate (vanadate) that inactivates p53 by inducing conformational change in it. Therefore, we investigated the effect of vanadate on the each pathways.
    We initially confirmed vanadate as an inhibitor of p53 transcription by luciferase reporter assay for its transcription and by immunoblotting of its transactivation. Furthermore, immunocoprecipitation analysis using anti-Bak, Bcl-2, and Bcl-xL antibodies demonstrated that vanadate suppressed the interaction of p53 with these Bcl-2 family proteins. Considering the evidence that these interacting proteins bind core domain of p53, vanadate may influence this domain, resulting in the inhibition of the binding of target genes and these protein partners.

    DOI: 10.11513/jrrsabst.2007.0.190.0

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  • Association of DNA-PK activity and radiation-induced NBS1 foci formation in lymphocytes with clinical malignancy in breast cancer patients Reviewed

    Someya, Masanori, Sakata, Koh-Ichi, Matsumot, Yoshihisa, Tauchi, Hiroshi, Narimatsu, Hideaki, Hareyama, Masato

    Oncology Reports   18 ( 4 )   873 - 878   2007

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    DOI: 10.3892/or.18.4.873

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  • CDNA analysis of gene expression associated with DNA-dependent protein kinase activity Reviewed

    Sakata, Koh-Ichi, Yamamoto, Hiroyuki, Matsumoto, Yoshihisa, Someya, Masanori, Hareyama, Masato

    International Journal of Oncology   30 ( 2 )   413 - 420   2007

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    DOI: 10.3892/ijo.30.2.413

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  • Ability to repair DNA double-strand breaks related to cancer susceptibility and radiosensitivity.

    Sakata, Koh-Ichi, Someya, Masanori, Matsumoto, Yoshihisa, Hareyama, Masato

    Radiation medicine   25 ( 9 )   433 - 8   2007

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    Traditional radiobiology has aimed at elucidating the mechanism of radiosensitivity of cancer cells and normal cells. Because the mechanism of DNA double-strand break (DSB) repair, which is inherently important to radiosensitivity, was unknown, it has been difficult to obtain results applicable to clinical radiotherapy from traditional radiobiology research. Today, however, the molecular mechanism of DNA DSB repair has been elucidated because of the rapid advances in molecular biology. In DNA DSB repair, at least two major repair mechanisms, homologous recombination and nonhomologous end joining (NHEJ) have been reported. In the NHEJ pathway, DSBs are directly, or after processing of the DNA ends, rejoined at an appropriate chromosomal end. DNA-dependent protein kinase (DNA-PK) plays an important role in DNA DSB repair by NHEJ. We have investigated how the ability of repair of DNA DSB influences cancer susceptibility and the radiosensitivity of tumors and normal tissues by focusing on the activity of DNA-PK. In the near future, research on DNA DSB repair mechanism will be able to be applied to research on carcinogenesis, prediction of radiosensitivity of tumors and normal cells, and sensitization of tumor cells.

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  • Immunohistochemical analysis of Ku70/86 expression of breast cancer tissues Reviewed

    Someya, Masanori, Sakata, Koh-ichi, Matsumoto, Yoshihisa, Satoh, Masaaki, Narimatsu, Hideaki, Hareyama, Masato

    Oncology Reports   18 ( 6 )   1483 - 1487   2007

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  • マイクロビームを用いた研究の進展 放射光X線マイクロビーム細胞照射装置を用いたDNA2本鎖切断修復タンパク質の可視化解析

    冨田 雅典, 前田 宗利, 宇佐美 徳子, 松本 義久, 小林 克己

    日本放射線影響学会大会講演要旨集   49回   83 - 83   2006.9

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  • 高LET放射線によるDNA損傷と細胞応答 高LET重イオンによるDNA損傷へのKu80の反応

    和田 成一, 松本 義久, 大戸 貴代, 浜田 信行, 原 孝光, 舟山 知夫, 坂下 哲哉, 深本 花菜, 柿崎 竹彦, 鈴木 芳代, 細井 義夫, 鈴木 紀夫, 小林 泰彦

    日本放射線影響学会大会講演要旨集   49回   73 - 73   2006.9

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  • Src tyrosine kinase inhibitor PP2 suppresses ERK1/2 activation and epidermal growth factor receptor transactivation by X-irradiation

    ZP Li, Y Hosoi, KS Cai, Y Tanno, Y Matsumoto, A Enomoto, A Morita, K Nakagawa, K Miyagawa

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   341 ( 2 )   363 - 368   2006.3

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    DOI: 10.1016/j.bbrc.2005.12.193

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  • Sodium orthovanadate suppresses DNA damage-induced caspase activation and apoptosis by inactivating p53

    A Morita, J Zhu, N Suzuki, A Enomoto, Y Matsumoto, M Tomita, T Suzuki, K Ohtomo, Y Hosoi

    CELL DEATH AND DIFFERENTIATION   13 ( 3 )   499 - 511   2006.3

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  • Association of ionizing radiation-induced foci of NBS1 with chromosomal instability and breast cancer susceptibility

    Someya, Masanori, Sakata, Koh-ichi, Tauchi, Hiroshi, Matsumoto, Yoshihisa, Nakamura, Asako, Komatsu, Kenshi, Hareyama, Masato

    Radiation Research   166 ( 4 )   575 - 582   2006

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    DOI: 10.1667/RR0638.1

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  • Recruitment and phosphorylation of NHEJ enzymes to DNA double-strand breaks

    MATSUMOTO Yoshihisa, BHOSLE Sushma M., TOMITA Masanori, ENOMOTO Atsushi, MORITA Akinori, SUZUKI Norio, HOSOI Yoshio, MIYAGAWA Kiyoshi

    The Japan Radiation Research Society Annual Meeting Abstracts   2006   140 - 140   2006

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    In eukaryotic cells, including mammal, DNA double strand breaks (DSBs) are repaired mainly through two pathways: non-homologous end-joining (NHEJ) and homologous recombination (HR). DNA-PK complex, composed of DNA-PKcs, Ku86 and Ku70, and XRCC4/DNA ligase IV complex have been considered key molecules in NHEJ but new molecule, XLF/Cernunnos was found very recently. It is largely unknown how these proteins are recruited to DSB sites and assembled into repair machinery. Another mystery is the role of protein phosphorylating function of DNA-PK. For our understanding of DSB repair mechanism through NHEJ, it is critically important i) to visualize and analyze the recruitment process of NHEJ molecules to DSBs and ii) to elucidate the genuine target of DNA-PKcs and the physiological significance of phosphorylation. Regarding this, we have reported the detection and characterization of DNA-PKcs foci induced by ionizing radiation and, this time, we successfully detected the binding of XRCC4 to damaged chromatin DNA. Additionally, we have identified the phosphorylation site of XRCC4 by DNA-PKcs, which is phosphorylated in living cells after irradiation and disruption of which resulted in elevated radiosensitivity with partially impaired DNA repair capability. Based on these results, the process of recruitment and assembly of NHEJ machinery and the role of DNA-PK phosphorylation therein will be discussed.

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  • Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC

    Hosoi, Yoshio, Kapp, Leon N., Murnane, John P., Matsumoto, Yoshihisa, Enomoto, Atsushi, Ono, Tetsuya, Miyagawa, Kiyoshi

    Biochemical and Biophysical Research Communications   348 ( 2 )   728 - 734   2006

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  • DNA切断センサーDNA-PKの性質と機能に関する研究-その成果は癌診断・治療にいかに生かせるか?

    松本義久

    癌と人   33   31 - 32   2006

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  • Not at the end of DNA double-strand break repair:新たに発見されたDNA二重鎖切断修復の重要分子XLF/Cernunnos

    松本義久

    放射線生物研究   42 ( 3 )   325 - 331   2006

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    Other Link: http://search.jamas.or.jp/link/ui/2007061026

  • 1P454 Localization of DNA double-strand break repair proteins in the target irradiated cell nuclei by synchrotron X-ray microbeam(20. Radiation biology,Poster Session,Abstract,Meeting Program of EABS &BSJ 2006)

    Tomita Masanori, Maeda Munetoshi, Usami Noriko, Matsumoto Yoshihisa, Kobayashi Katsumi

    Seibutsu Butsuri   46 ( 2 )   S260   2006

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    DOI: 10.2142/biophys.46.S260_2

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  • Heterogeneous expression of DNA-dependent protein kinase in esophageal cancer and normal epithelium

    Tonotsuka, Norio, Hosoi, Yoshio, Miyazaki, Shukichi, Miyata, Go, Sugawara, Ko, Mori, Takahiro, Ouchi, Noriaki, Satomi, Susumu, Matsumoto, Yoshihisa, Nakagawa, Keiichi, Miyagawa, Kiyoshi, Ono, Tetsuya

    International Journal of Molecular Medicine   18 ( 3 )   441 - 447   2006

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  • The association of DNA-dependent protein kinase activity with chromosomal instability and risk of cancer

    Someya, M, Sakata, K, Matsumoto, Y, Yamamoto, H, Monobe, M, Ikeda, H, Ando, K, Hosoi, Y, Suzuki, N, Hareyama, M

    Carcinogenesis   27 ( 1 )   117 - 122   2006

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    DOI: 10.1093/carcin/bgi175

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  • Transcriptional regulation of DNA double-strand break repair genes by Sp1

    HOSOI Yoshio, TANNO Yuuji, MATSUMOTO Yoshihisa, ENOMOTO Atsushi, KATURA Mari, TAKAKURA Kaoru, MIYAGAWA Kiyoshi

    The Japan Radiation Research Society Annual Meeting Abstracts   2006   95 - 95   2006

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    DNA-dependent protein kinase (DNA-PK) is involved in DNA double-strand breaks (DSBs) repair, and it consists of Ku70, Ku80 and DNA-PKcs. It has been shown that the promoter regions of these three genes have Sp1 binding sites, and the expression levels are correlated with that of Sp1. The purpose of this study is to clarify the contribution of Sp1 to radiation sensitivity of cells through the transcriptional regulation of DSBs-repair genes. We investigated whether Sp1 affects the protein and mRNA levels of Ku70, Ku80, DNA-PKcs, XRCC4, NBS1, MRE11 and MDC1. In addition, we examined the DSBs-repair, DNA-PK activity, cell cycle, and radiation sensitivity in Sp1-dawn-regulated cells. A human transformed kidney cell line 293T was transfected with siRNA vector targeting Sp1 (Sp1-siRNA) or control vector. The vector-transfected cells were selected with G418. After 7 days selection, protein and mRNA levels were evaluated by Western blotting and RT-PCR, respectively. The protein and mRNA levels of Sp1, Ku70, Ku80, DNA-PKcs, XRCC4, NBS1, MRE11 and MDC1 were down regulated by the Sp1-siRNA treatment. The DSBs-repair after 80 Gy irradiation and DNA-PK activity were suppressed by the Sp1-siRNA treatment. The surviving fraction after irradiation was also suppressed by the Sp1-siRNA treatment. However, cell cycle was not affected by the Sp1-siRNA treatment. These results suggest that Sp1 regulates the radiation sensitivity by the transcriptional regulation of DSBs-repair genes.

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  • Analysis of a novel regulator in JNK cascade and the application for apoptosis

    ENOMOTO Atsushi, KIDO Naoki, MORITA Akinori, ITO Michihiko, MATSUMOTO Yoshihisa, HOSOI Yoshio, MIYAGAWA Kiyoshi

    The Japan Radiation Research Society Annual Meeting Abstracts   2006   204 - 204   2006

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    The mitogen-activated protein kinase (MAPK) cascades, in which the components are MAPK, MAPKK, MAPKKK, are conserved in eukaryotic signaling pathways. The general function of the MAPK cascades is to link a variety of extracellular stimuli to nuclear responses, i.e., the modulation of gene expression. In mammals, at least three MAPK cascades have been identified. The MAPKs in each pathway are JNK, p38, or ERK. Especially, JNK cascades are known to regulate stress responses and apoptosis. We successfully identified a novel serine-threonine kinase (STK) binding to MAPKKK such as MEKK1, MEKK2, or TAK1 in JNK cascade. The roles and substrates of the STK in cells are unknown. Overexpression of the STK inhibits the activation of MEKK1 or MEKK2. Then, we constructed the sh RNA expression vector for the STK and introduced into HELA cells. Knock-down of the STK led to the enhancement of MAPKKK activity and of stress-induced apoptosis.

    DOI: 10.11513/jrrsabst.2006.0.204.0

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  • Response of Ku80 to DNA damage induced by high LET heavy ions

    WA S, MATSUMOTO Yoshihisa, OOTO Takayo, HAMADA Nobuyuki, HARA Takamitsu, FUNAYAMA Tomoo, SAKASHITA Tetsuya, FUKAMOTO Kana, KAKIZAKI Takehiko, SUZUKI Michiyo, HOSOI Yoshio, SUZUKI Norio, KOBAYASHI Yasuhiko

    The Japan Radiation Research Society Annual Meeting Abstracts   2006   33 - 33   2006

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    It is well known that high-LET heavy ion is more effective for lethal effect than low LET radiation. It is considered that this high effectiveness is caused by heavy ion-induced clustered DNA damages, which are thought to be non-repairable or difficult to be repaired. However, much less is known about difficultly of clustered DNA damages repair in DNA repair process. The major DNA repair pathway in mammalian cells is non-homologous end joining (NHEJ). In this study we investigated NHEJ pathway by analyzing responses of Ku to DNA damage induced by high-LET heavy ions. pGFP and pGFP-Ku80 were transfected into Ku80-defective xrs-5 cells. Cells were irradiated with 7.2 MeV /u Ar13+beams (LET=1610 keV/μm) at TIARA JAEA-Takasaki. Sensitivity of Xrs5-GFP-Ku80 cells and xrs5-GFP cells to Ar13+was comparable. This result indicates that DNA damage induced by Ar13+is difficult to be repaired. To evaluate the response of Ku80 to DNA damage induced by heavy ions, GFP and γH2AX foci in the nuclei were observed. These foci were co-localized at 10 min after irradiation, while GFP foci were not clear and co-localized signal were not observed at 20 min. it was inferred that Ku proteins recognized DNA damage induced by Ar ions and dissociate from DNA ends without repair.

    DOI: 10.11513/jrrsabst.2006.0.33.0

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  • Retardation of removal of radiation-induced apoptotic cells in developing neural tubes in macrophage galactose-type C-type lectin-1-deficient mouse embryos

    H Yuita, M Tsuiji, Y Tajika, Y Matsumoto, K Hirano, N Suzuki, T Irimura

    GLYCOBIOLOGY   15 ( 12 )   1368 - 1375   2005.12

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  • 高LET重イオンによるDNA損傷の非相同性末端結合による修復の解析

    和田 成一, 舟山 知夫, 松本 義久, 大戸 貴代, 坂下 哲哉, 浜田 信行, 横田 裕一郎, 柿崎 竹彦, 細井 義夫, 鈴木 紀夫, 小林 泰彦

    日本放射線影響学会大会講演要旨集   48回   115 - 115   2005.11

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  • Prognostic significance of Ku70 protein expression in patients with advanced colorectal cancer

    Y Komuro, T Watanabe, Y Hosoi, Y Matsumoto, K Nakagawa, N Suzuki, H Nagawa

    HEPATO-GASTROENTEROLOGY   52 ( 64 )   995 - 998   2005.7

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  • DNA二重鎖切断センサー:DNA依存性プロテインキナーゼ(DNA-PK)機能研究の現状と課題

    松本義久

    放射線生物研究   40 ( 2 )   82 - 108   2005

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  • Radiosensitization by hyperthermia in the chicken B-lymphocyte cell line DT40 and its derivatives lacking nonhomologous end joining and/or homologous recombination pathways of DNA double-strand break repair

    HL Yin, Y Suzuki, Y Matsumoto, M Tomita, Y Furusawa, A Enomoto, A Morita, M Aoki, F Yatagai, T Suzuki, Y Hosoi, K Ohtomo, N Suzuki

    RADIATION RESEARCH   162 ( 4 )   433 - 441   2004.10

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  • Suramin sensitizes cells to ionizing radiation by inactivating DNA-dependent protein kinase

    Y Hosoi, Y Matsumoto, A Enomoto, A Morita, J Green, K Nakagawa, K Naruse, N Suzuki

    RADIATION RESEARCH   162 ( 3 )   308 - 314   2004.9

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    DOI: 10.1667/RR3217

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  • Up-regulation of DNA-dependent protein kinase activity and Sp1 in colorectal cancer

    Hosoi, Y, Watanabe, T, Nakagawa, K, Matsumoto, Y, Enomoto, A, Morita, A, Nagawa, H, Suzuki, N

    International Journal of Oncology   25 ( 2 )   461 - 468   2004

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  • Potentiality of DNA-dependent protein kinase to phosphorylate Ser46 of human p53

    Komiyama, S, Taniguchi, S, Matsumoto, Y, Tsunoda, E, Ohto, T, Suzuki, Y, Yin, HL, Tomita, M, Enomoto, F, Morita, A, Suzuki, T, Ohtomo, K, Hosoi, Y, Suzuki, N

    Biochemical and Biophysical Research Communications   323 ( 3 )   816 - 822   2004

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    DOI: 10.1016/j.bbrc.2004.08.161

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  • Decreased c-Myc expression and its involvement in X-ray-induced apoptotic cell death of human T-cell leukaemia cell line MOLT-4

    A Enomoto, N Suzuki, Y Kang, K Hirano, Y Matsumoto, J Zhu, A Morita, Y Hosoi, K Sakai, H Koyama

    INTERNATIONAL JOURNAL OF RADIATION BIOLOGY   79 ( 8 )   589 - 600   2003.8

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    DOI: 10.1080/09553000310001597273

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  • Caspase-mediated cleavage of JNK during stress-induced apoptosis

    A Enomoto, N Suzuki, A Morita, M Ito, CQ Liu, Y Matsumoto, K Yoshioka, T Shiba, Y Hosoi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   306 ( 4 )   837 - 842   2003.7

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    DOI: 10.1016/S0006-291X(03)01050-7

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  • Difference in the heat sensitivity of DNA-dependent protein kinase activity among mouse, hamster and human cells

    Umeda, N, Matsumoto, Y, Yin, HL, Tomita, M, Enomoto, A, Morita, A, Mizukoshi, T, Sakai, K, Hosoi, Y, Suzuki, N

    International Journal of Radiation Biology   79 ( 8 )   671 - 680   2003

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    DOI: 10.1080/09553000310001596959

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  • Wortmannin-enhanced X-ray-induced apoptosis of human T-cell leukemia MOLT-4 cells possibly through the JNK/SAPK pathway

    Tomita, M, Suzuki, N, Matsumoto, Y, Enomoto, A, Yin, HL, Hosoi, Y, Hirano, K, Sakai, K

    Radiation Research   160 ( 4 )   467 - 477   2003

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  • Prediction of tumor radiosensitivity in rectal carcinoma based on p53 and Ku70 expression

    Komuro, Y, Watanabe, T, Hosoi, Y, Matsumoto, Y, Nakagawa, K, Saito, S, Ishihara, S, Kazama, S, Tsuno, N, Kitayama, J, Suzuki, N, Tsurita, G, Muto, T, Nagawa, H

    Journal of Experimental &amp; Clinical Cancer Research   22 ( 2 )   223 - 228   2003

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  • Phosphorothioate oligonucleotides, suramin and heparin inhibit DNA-dependent protein kinase activity

    Y Hosoi, Y Matsumoto, M Tomita, A Enomoto, A Morita, K Sakai, N Umeda, HJ Zhao, K Nakagawa, T Ono, N Suzuki

    BRITISH JOURNAL OF CANCER   86 ( 7 )   1143 - 1149   2002.4

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    DOI: 10.1038/sj/bjc/6600191

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  • Phosphorothioate oligonucleotides, suramin and heparin inhibit DNA-dependent protein kinase activity Reviewed

    Hosoi, Y, Matsumoto, Y, Tomita, M, Enomoto, A, Morita, A, Sakai, K, Umeda, N, Zhao, HJ, Nakagawa, K, Ono, T, Suzuki, N

    British Journal of Cancer   86 ( 7 )   1143 - 1149   2002

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    DOI: 10.1038/sj/bjc/6600191

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  • Roles of DNA-dependent protein kinase and ATM in cell-cycle-dependent radiation sensitivity in human cells

    Yoshida, M, Hosoi, Y, Miyachi, H, Ishii, N, Matsumoto, Y, Enomoto, A, Nakagawa, K, Yamada, S, Suzuki, N, Ono, T

    International Journal of Radiation Biology   78 ( 6 )   503 - 512   2002

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    DOI: 10.1080/095530002317577321

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  • The expression pattern of Ku correlates with tumor radiosensitivity and disease free survival in patients with rectal carcinoma

    Komuro, Y, Watanabe, T, Hosoi, Y, Matsumoto, Y, Nakagawa, K, Tsuno, N, Kazama, S, Kitayama, J, Suzuki, N, Nagawa, H

    Cancer   95 ( 6 )   1199 - 1205   2002

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    DOI: 10.1002/cncr.10807

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  • Induction of interleukin-1 beta and interleukin-6 mRNA by low doses of ionizing radiation in macrophages

    Hosoi, Y, Miyachi, H, Matsumoto, Y, Enomoto, A, Nakagawa, K, Suzuki, N, Ono, T

    International Journal of Cancer   96 ( 5 )   270 - 276   2001

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    DOI: 10.1002/ijc.1030

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  • Involvement of c-Jun NH2-terminal kinase-1 in heat-induced apoptotic cell death of human monoblastic leukaemia U937 cells

    Enomoto, A, Suzuki, N, Liu, C, Kang, Y, Zhu, J, Serizawa, S, Matsumoto, Y, Morita, A, Ito, M, Hosoi, Y

    International Journal of Radiation Biology   77 ( 8 )   867 - 874   2001

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    DOI: 10.1080/09553000110062512

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  • Expression of genes involved in repair of DNA double-strand breaks in normal and tumor tissues

    Sakata, KI, Matsumoto, Y, Tauchi, H, Satoh, M, Oouchi, A, Nagakura, H, Koito, K, Hosoi, Y, Suzuki, N, Komatsu, K, Hareyama, M

    International Journal of Radiation Oncology Biology Physics   49 ( 1 )   161 - 167   2001

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    DOI: 10.1016/S0360-3016(00)01352-3

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  • Clinical studies of immunohistochemical staining of DNA-dependent protein kinase in oropharyngeal and hypopharyngeal carcinomas.

    Sakata, K, Matsumoto, Y, Satoh, M, Oouchi, A, Nagakura, H, Koito, K, Hosoi, Y, Hareyama, M, Suzuki, N

    Radiation medicine   19 ( 2 )   93 - 97   2001

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  • Variations in Prkdc encoding the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) and susceptibility to radiation-induced apoptosis and lymphomagenesis

    Mori, N, Matsumoto, Y, Okumoto, M, Suzuki, N, Yamate, J

    Oncogene   20 ( 28 )   3609 - 3619   2001

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    DOI: 10.1038/sj.onc.1204497

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  • イノシトールヘキサキスリン酸がDNA2重鎖切断の修復に関与する!?

    松本義久

    放射線生物研究   38 ( 1 )   70 - 73   2001

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  • DNA依存性プロテインキナーゼの性質と放射線感受性-DNA-PKの温熱不安定性と温熱の放射線増感効果について-

    松本義久, 梅田典子, 冨田雅典, 細井義夫, 鈴木紀夫

    癌の臨床   47   3 - 7   2001

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  • Sensitization by wortmannin of heat- or X-ray induced cell death in cultured Chinese hamster V79 cells

    M Tomita, N Suzuki, Y Matsumoto, K Hirano, N Umeda, K Sakai

    JOURNAL OF RADIATION RESEARCH   41 ( 2 )   93 - 102   2000.6

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    DOI: 10.1269/jrr.41.93

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  • Involvement of SAPK/JNK pathway in X-ray-induced rapid cell death of human T-cell leukemia cell line MOLT-4

    Enomoto, A, Suzuki, N, Hirano, K, Matsumoto, Y, Morita, A, Sakai, K, Koyama, H

    Cancer Letters   155 ( 2 )   137 - 144   2000

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    DOI: 10.1016/S0304-3835(00)00422-5

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  • Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation

    Matsumoto, Y, Suzuki, N, Namba, N, Umeda, N, Ma, XJ, Morita, A, Tomita, M, Enomoto, A, Serizawa, S, Hirano, K, Sakai, K, Yasuda, H, Hosoi, Y

    Febs Letters   478 ( 1-2 )   67 - 71   2000

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    DOI: 10.1016/S0014-5793(00)01800-7

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  • Involvement of SAPK/JNK pathway in X-ray-induced apoptosis of human T-cell leukemia cell line MOLT-4

    Enomoto, Atsushi, Hirano, Kazuya, Matsumoto, Yoshihisa, Hosoi, Yoshio, Koyama, Hideki, Sakai, Kazuo, Suzuki, Norio

    Journal of Radiation Research   41 ( 4 )   410 - 410   2000

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  • p41 as a possible marker for cell death is generated by caspase cleavage of p42/SET beta in irradiated MOLT-4 cells

    Morita, A, Suzuki, N, Matsumoto, Y, Hirano, K, Enomoto, A, Zhu, J, Sakai, K

    Biochemical and Biophysical Research Communications   278 ( 3 )   627 - 632   2000

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    DOI: 10.1006/bbrc.2000.3860

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  • A gel-electrophoretic analysis for improved sensitivity and specificity of DNA-dependent protein kinase activity

    Matsumoto, Y, Umeda, N, Suzuki, N, Sakai, K, Hirano, K

    Journal of Radiation Research   40 ( 2 )   183 - 196   1999

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    DOI: 10.1269/jrr.40.183

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  • A phosphatidylinositol 3-kinase inhibitor wortmannin induces radioresistant DNA synthesis and sensitizes cells to bleomycin and ionizing radiation

    Hosoi, Y, Miyachi, H, Matsumoto, Y, Ikehata, H, Komura, J, Ishii, K, Zhao, HJ, Yoshida, M, Takai, Y, Yamada, S, Suzuki, N, Ono, T

    International Journal of Cancer   78 ( 5 )   642 - 647   1998

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    DOI: 10.1002/(SICI)1097-0215(19981123)78:5<642::AID-IJC19>3.0.CO;2-3

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  • A possible mechanism for hyperthermic radiosensitization mediated through hyperthermic lability of Ku subunits in DNA-dependent protein kinase

    Matsumoto, Y, Suzuki, N, Sakai, K, Morimatsu, A, Hirano, K, Murofushi, H

    Biochemical and Biophysical Research Communications   234 ( 3 )   568 - 572   1997

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    DOI: 10.1006/bbrc.1997.6689

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  • DNA依存性プロテインキナーゼ(DNA-PK)とその放射線応答における意義-The end is the beginning of the story.-

    松本義久

    放射線生物研究   31   1 - 27   1996

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  • Identification and characterization of a protein found after X-irradiation in human T cell leukemia

    Morimatsu, A, Suzuki, N, Hirano, K, Matsumoto, Y, Sakai, K

    Journal of Radiation Research   37 ( 1 )   1 - 11   1996

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    DOI: 10.1269/jrr.37.1

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Books

  • 原子力年鑑2020

    MATSUMOTO Yoshihisa( Role: Contributorコラム2 低線量放射線照射の人体への影響のミクロな機構)

    日刊工業新聞社  2019.11 

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    Responsible for pages:97-98   Language:Japanese   Book type:Dictionary, encyclopedia

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  • 放射線生物学の事典

    松本 義久( Role: Contributor2.4 放射線によるDNA損傷の修復)

    朝倉書店  2019.10 

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    Total pages:300   Language:Japanese   Book type:Dictionary, encyclopedia

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  • Recent Trends and Advances in Environmental Health

    Samarth RM, Kumar M, Matsumoto Y, Manda K( Role: Joint authorThe Effects of Ionizing and Non-Ionizing Radiation on Health)

    Nova Science Publishers  2019.7 

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  • 人体のメカニズムから学ぶ 放射線生物学

    松本 義久( Role: Edit)

    メジカルビュー社  2017.2 

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    Total pages:315   Language:Japanese   Book type:Textbook, survey, introduction

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  • 新版 放射線医科学–生体と放射線•電磁波・超音波-

    松本 義久( Role: Contributor1.4 放射線によるDNA損傷の修復)

    医療科学社  2016.10 

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    Total pages:189   Responsible for pages:17-19   Language:Japanese   Book type:Textbook, survey, introduction

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  • 本当のところを教えて! 放射線のリスク 放射線影響研究者からのメッセージ

    宇佐美 徳子, 柿沼 志津子, 島田 義也, 鈴木 啓司, 田内 広, 松本 英樹, 松本 義久, 三谷 啓志, 渡邉 正己( Role: Joint author)

    医療科学社  2015.1 

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    Total pages:129   Language:Japanese   Book type:Scholarly book

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  • Biological Responses, Monitoring and Protection from Radiation Exposure

    MATSUMOTO Yoshihisa( Role: ContributorRadiation Monitoring and Radioprotection in Nuclear Disaster: Lessons from Fukushima Daiichi Nuclear Power Plant Accident)

    Nova Scientific Publishers  2014.7 

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  • 臨床放射線腫瘍学

    日本放射線腫瘍学会, 日本放射線腫瘍学研究機構編( Role: Contributor放射線によるDNA損傷・修復と細胞死)

    南江堂  2012.12 

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    Total pages:522   Responsible for pages:40-44   Language:English   Book type:Textbook, survey, introduction

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  • Emerging Trends in Zoology

    Kumar A, Matsumoto Y( Role: Joint authorRadiation protection by herbs and plants)

    Narendra Publishing House  2011.7 

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  • 放射線医科学 –生体と放射線•電磁波・超音波-

    松本 義久( Role: Contributor放射線によるDNA損傷の修復)

    学会出版センター  2007.3 

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    Total pages:148   Responsible for pages:18-21   Language:Japanese   Book type:Textbook, survey, introduction

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MISC

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Presentations

  • 放射線生物学の基礎:細胞死について考える Invited

    松本義久

    日本放射線腫瘍学会第38回学術大会  2025.11 

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    Event date: 2025.11

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

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  • ゴジラとともにシン化する放射線生物学

    松本義久

    日本量子医科学会第5回学術大会  2025.11 

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    Event date: 2025.11

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

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  • Nuclear 3S (Safety, Security, and Safeguards) Education Program Invited

    Chi Young Han, Hiroshi Sagara, Yoshihisa Matsumoto

    International Nuclear Security Education Network (INSEN) Annual Meeting  2025.11 

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    Event date: 2025.11

    Language:English   Presentation type:Oral presentation (invited, special)  

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  • Radiation risk communication to elementary and middle school students: an approach to verify the effectiveness of organizational collaboration

    Hiroshi Tauchi, Atsushi Kaida, Norie Kanzaki, Ryuji Okazaki, Asako, J Nakamura, Masami Watanabe, Yoshihisa Matsumoto

    6th Asian Congree of Radiation Research / 68th Japanese Radiation Research Society  2025.10 

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    Event date: 2025.10

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  • Study on the impact of A247S variant in XRCC4 on DNA double-strand break repair and radiation sensitivity

    Mando Amanda Lynn Eijansantos, Rikiya Imamura, Hisanori Tazuru, Kaima Tsukada, Mikio Shimada, Yoshihisa Matsumoto

    6th Asian Congree of Radiation Research / 68th Japanese Radiation Research Society  2025.10 

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  • A mathematical formulation to describe clonogenic cell survival under low dose rate irradiation

    Yoshihisa Matsumoto

    8th International Symposium on the System of Radiation Protection (ICRP2025)  2025.10 

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    Event date: 2025.10

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  • Work in Progress of Working Groups of PLANET in Japan

    Yutaka Yamada, Tatsuhiko Imaoka, Toshiyasu Iwasaki, Junya Kobayashi, Toshiyuki Kobayashi, Munechika Misumi, Tetsuya Ohira, Kazuo Sakai, Takashi Sugihara, Keiji Suzuki, Hiroshi Tauchi, Hiroshi Yasuda, Shinji Yoshinaga, Kazutaka Doi, Megumi Sasatani, Masanori Tomita, Atsushi Kohda, Yoshihisa Matsumoto, Daisuke Iizuka, Kazuhiro Daino, Yuki Fujimichi, Asako Nakamura, Mitsuaki Ojima, Tokuhisa Hirouchi, Kensuke Otsuka, Chizuru Tsuruoka, Shizuko Kakinuma, Michiya Sasaki, Michiaki Kai

    8th International Symposium on the System of Radiation Protection (ICRP2025)  2025.10 

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    Event date: 2025.10

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  • 放射線生物学からの宇宙における健康・医療へのアプローチ Invited

    松本義久

    第86回応用物理学会秋季学術講演会  2025.9 

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    Event date: 2025.9

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

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  • Examination of cell experiments for boron neutron capture therapy using the reactor in Kindai University

    2025.7 

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    Event date: 2025.7

    Language:Japanese   Presentation type:Poster presentation  

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  • DNA二重鎖切断の認識と修復:分子メカニズムからがん治療へ Invited

    松本義久

    第1525回生物科学セミナー  2025.7 

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    Event date: 2025.7

    Language:Japanese   Presentation type:Public lecture, seminar, tutorial, course, or other speech  

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  • ヒト神経組織における放射線影響と防護作用の研究

    島田 幹男, 松本 義久

    第62回アイソトープ・放射線研究発表会  2025.7 

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    Event date: 2025.7

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • シン・ゴジラの放射線感受性:DNA-PKに関するリアルとフィクションのコンバージェンス

    松本 義久

    第29回癌治療増感研究会  2025.6 

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    Event date: 2025.6

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • 「核」と「核」をつなぐ:医歯理工連携の中での放射線生物学の立ち位置 Invited

    松本 義久

    第53回放射線による制癌シンポジウム  2025.5 

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    Event date: 2025.5

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  • DNA修復酵素Polynucleotide kinase phosphatase(PNKP)の岡崎フラグメントのギャップ間結合における新規機能〜抗がん剤の分子標的としての可能性〜

    島田 幹男, 塚田 海馬, 今村 力也, Fu Linyang, 三宅 智子, 松本 義久

    第62回日本放射線腫瘍学会生物部会学術大会  2025.5 

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  • 日本人由来EBV不死化リンパ球におけるDNA二本鎖切断修復遺伝子XRCC4一塩基多型の解析

    吉田 和起, 島田 幹男, 松本 義久

    第25回菅原・大西記念癌治療増感シンポジウム  2025.2 

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    Event date: 2025.2

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  • Recognition and Repair of DNA Double-strand Breaks: Seeking for Molecular Mechanisms and Its Implication for Cancer Therapy and Radioprotection in Next Generation

    Yoshihisa Matsumoto, Mikio Shimada

    International Symposium on Green Transformation Initiative and Innovative Zero-Carbon Energy Systems  2025.1 

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    Event date: 2025.1

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  • Optimizing Dose Evaluation of Targeted Alpha Therapy with Experiments and Simulation

    Yumin Huang, Tetsuya Sakashita, Yasuhiro Ohshima, Ichiro Sasaki, Noriko S. Ishioka, Yoshihisa Matsumoto

    International Symposium on Green Transformation Initiative and Innovative Zero-Carbon Energy Systems  2025.1 

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    Event date: 2025.1

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  • Deciphering the mechanisms of PNKP regulation toward improvement of cancer radiotherapy

    Lingyan Fu, Rikiya Imamura, Tomoko Miyake, Kaima Tsukada, Yoshihisa Matsumoto, Mikio Shimada

    International Symposium on Green Transformation Initiative and Innovative Zero-Carbon Energy Systems  2025.1 

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    Event date: 2025.1

    Language:English   Presentation type:Oral presentation (general)  

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  • Basic Mechanisms for DNA Double-strand Break Repair Invited

    Yoshihisa Matsumoto

    Second International School on Radiation Research (ISRR-2020)  2020.9 

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    Event date: 2020.9

    Language:English   Presentation type:Oral presentation (invited, special)  

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  • XRCC4 phosphorylation as an in situ indicator for DNA-PK activity International conference

    Mukesh Kumar Sharma, Ali Reza Amiri Moghani, Mikoto Fukuchi, Shoji Imamichi, Anie Day Asa De Castro, Rujira Wanotayan, Mikio Shimada, Yoshihisa Matsumoto

    The 12th International conference & 5th Asian Congress on Environmental Mutagens  2017.11 

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:Songdo Convensia (Incheon, Korea)  

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  • Fukushima Daiichi Nuclear Power Plant Accident from the Aspect of Radiation Biologist II Countermeasures and Social Responsibilities Invited International conference

    Matsumoto, Y

    International Conference on Radiation, Cancer and Society  2012.11 

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    Venue:Allahabad (Auditorium, Vigyan, Parisad), India  

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  • Implication of DNA double-strand break repair in cancer, aging and development International conference

    Yoshihisa Matsumoto

    The 12th International conference & 5th Asian Congress on Environmental Mutagens  2017.11 

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    Venue:Songdo Convensia (Incheon, Korea)  

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  • Fukushima Daiichi Nuclear Power Plant Accident from the Aspect of Radiation Biologist Invited International conference

    Matsumoto, Y

    International Conference on Radiation, Cancer and Society  2012.11 

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    Venue:Allahabad (Auditorium, Vigyan, Parisad), India  

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  • プラズマバブル水による皮膚常在菌の不活化とヒト培養細胞への影響調査

    細田 順平, 川野 浩明, 三宅 智子, 島田 幹男, 松村 有里子, 宮原 秀一, 松本 義久, 岩澤 篤郎, 沖野 晃俊

    Plasma Conference 2017 (PLASMA2017)  2017.11 

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:姫路商工会議所  

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  • Role of BRCT domains of DNA Ligase IV in its chromatin binding and recruitment of XRCC4 International conference

    Liu, S, Kamdar, R.P, Adachi, N, Matsumoto, Y

    28th RBC-NIRS International Symposium  2012.11 

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    Venue:Kyoto (Coop-Inn Kyoto)  

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  • 医学、_命科学における放射線利_の現状と可能性 Invited

    松本 義久

    公益財団法人若狭湾エネルギー研究センター第19回研究報告会  2017.10 

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    Language:Japanese   Presentation type:Oral presentation (keynote)  

    Venue:福井大学文京キャンパス  

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  • 原子力合意形成学に関する一考察(IV):低線量影響に対するリスクコミュニケーション

    山野 直樹, 安田 仲宏, 林崎 規託, 松本 義久

    日本原子力学会2012年秋の大会  2012.9 

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    Venue:広島大学東広島キャンパ  

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  • Structural analysis of DNA repair protein XRCC4 applying circular dichroism in an aqueous solution International conference

    Kai Nishikubo, Yudai Izumi, Yoshihisa Matsumoto, Akinari Yokoya

    Micros 2017- 17th International Symposium on Microdosimetry  2017.11 

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    Venue:Congress Center Cultural Center Don Orione Artigianelli (Venice, Italy)  

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  • Investigation of sterilization and biological effect using temperature controllable multi-gas plasma jet source International conference

    Takamatsu T, Oshita T, Kawate A, Uehara K, Nakashima N, Miyahara H, Matsumoto Y, Okino A

    34th International Symposium on Dry Process  2012.11 

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    Venue:The University of Tokyo  

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  • Fukushima Daiichi Nuclear Power Plant Accident from the Aspect of Radiation Biologist. Invited International conference

    Matsumoto, Y

    International Conference of Radiation Biology 2012  2012.11 

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    Venue:Advanced Centre for Treatment, Research and Education of Cancer, Navi Mumbai, India  

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  • ヒト細胞におけるヒストンシャペロンAsf1のDNA損傷応答の解析

    山崎 あかね, 島田 幹男, 松本 義久

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • Chromatin binding of XRCC4-DNA ligase IV complex revealed by biochemical fractionation analysis

    Sicheng LIU, Radhika Pankaj KAMDAR, 足立 典隆, 松本 義久

    日本放射線影響学会第55回大会  2012.9 

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    Venue:東北大学  

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  • iPS細胞における放射線応答機構と細胞周期チェックポイントの解析

    島田 幹男, 松本 義久

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • The fidelity of the repair of DNA damage by neutron irradiation and its dependence on XRCC4 status

    今道 祥二, 松本 義久

    日本放射線影響学会第55回大会  2012.9 

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    Venue:東北大学  

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  • DNA損傷応答可視化へ向けたGFP-p53融合タンパク質の発現と挙動の解析

    塚田 海馬, 島田 幹男, 松本 義久

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • Analysis of XRCC4 phosphorylation in vitro and in cellulo by DNA-PK

    Mukesh Kumar SHARMA, Rujira WANOTAYAN, 福地 命, 今道 祥二, 松本 義久

    日本放射線影響学会第55回大会  2012.9 

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    Venue:東北大学  

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  • 原子核・原子力理工学分野における放射線生物学の課題と挑戦

    松本 義久

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • 大気圧混合ガスプラズマを用いた高効率殺菌と生体への影響調査

    高松 利寛, 大下 貴也, 上原 広大, 川手 彬嗣, 宮原 秀一, 松本 義久, 沖野 晃俊

    第39回日本防菌防黴学会年次大会  2012.9 

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    Venue:きゅりあん(東京)  

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  • シンクロトロン放射を用いたCDスペクトル測定によるDNA修復タンパク質XRCC4の溶液中での構造解析

    西久保 開, 泉 雄大, 藤井 健太郎, 松本 義久, 横谷 明徳

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • DNA二重鎖切断修復欠損細胞の低線量率放射線に対する応答の解析

    土屋 尚代, 島田 幹男, 小林 純也, 松本 義久

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • Irradiation effect of temperature controlled 20℃ multi-gas plasma on bacteria and human cell International conference

    Takamatsu T, Oshita T, Kawate A, Uehara K, Nakashima N, Miyahara H, Matsumoto Y, Okino A

    9th International Bioelectrics Symposium  2012.9 

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    Venue:KKR Hotel Kumamoto  

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  • DNA double-strand break repair and V(D)J recombination function of XRCC4 mutants with microcephaly and growth defect

    Anie Day ASA, Rujira WANOTAYAN, Mikio SHIMADA, Yoshihisa MATSUMOTO

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • アポトーシスで生じたXRCC4N末断片による非DNA損傷性アポトーシスの制御機構

    橋本 優実, Radhika Pankaj KAMDAR, Mukesh Kumar SHARMA, 松井 理, 橋本 光正, 松本 義久, 岩淵 邦芳

    日本放射線影響学会第55回大会  2012.9 

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    Venue:東北大学  

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  • DNA複製におけるDNA修復因子Polynucleotide kinase phosphatase (PNKP)の機能解析と抗がん剤への応用

    加瀬 直也, 島田 幹男, 中野 洋文, 中村 浩之, 松本 義久

    日本放射線影響学会第60回大会  2017.10 

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    Venue:京葉銀行文化プラザ  

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  • 低線量率放射線照射下におけるDNA二重鎖切断修復因子の役割

    冨田 雅典, 小林 純也, 岩淵 邦芳, 松本 義久, 足立 典隆, 高田 穣, 内海 博司

    日本放射線影響学会第55回大会  2012.9 

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    Venue:東北大学  

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  • 生体内でのDNA損傷応答可視化に向けたGFP-p53融合タンパク質の発現・挙動解析

    塚田 海馬, 島田 幹男, 松本 義久

    若手放射線生物学研究会主催平成29年度専門研究会  2017.9 

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    Venue:東京大学アイソトープ総合センター  

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  • 低濃度エダラボンによる放射線増感効果

    笹野 仲史, 榎本 敦, 細井 義夫, 松本 義久, 勝村 庸介, 森田 明典, 宮川 清, 中川 恵一

    第47回日本医学放射線学会生物部会学術大会  2012.6 

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    Venue:高知(ホテル日航高知旭ロイヤル)  

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  • Behavior of DNA double-strand break repair-deficient cells under low dose rate irradiation

    Yoshihisa Matsumoto, Hisayo Tsuchiya, Mikio Shimada, Junya Kobayashi

    第76回日本癌学会学術総会  2017.9 

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    Venue:パシフィコ横浜  

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  • Temperature controllable cold plasma source for medical application International conference

    Oshita T, Takamatsu T, Nakashima N, Miyahara H, Matsumoto Y, Okino A

    The 39th IEEE International Conference on Plasma Science  2012.7 

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    Venue:Edinburgh International Conference Centre (Edinburgh, United Kingdom)  

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  • DNA double-strand break repair and V(D)J recombination function of XRCC4 mutants associated with microcephaly and growth defect International conference

    Anie Day, Dc. Asa, Rujira Wanotayan, Mikio Shimada, Yoshihisa Matsumoto

    63rd Annual International Meeting of Radiation Research Society  2017.10 

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    Venue:Grand Fiesta America, Coral Beach (Cancun, Mexico)  

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  • DNA二本鎖切断修復タンパク質XRCC4を介したアポトーシス制御機構の解明

    橋本 優実, Radhika Pankaj KAMDAR, Mukesh Kumar SHARMA, 松井 理, 橋本 光正, 松本 義久, 岩淵 邦芳

    金沢医科大学医学会第48回学術集会  2012.7 

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    Venue:金沢医科大学  

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  • Investigation of sterilization effect of plasma gas temperature using temperature controllable plasma jet International conference

    Oshita T, Takamatsu T, Uehara K, Kawate A, Nakashima N, Miyahara H, Matsumoto Y, Okino A

    9th International Bioelectrics Symposium  2012.9 

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    Venue:KKR Hotel Kumamoto  

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  • Identification of the phosphorylation sites of XRCC4 by DNA-PK essential for DNA double-strand break repair

    Mukesh Kumar SHARMA, Shoji IMAMICHI, Radhika Pankaj KAMDAR, Mikoto FUKUCHI, Sicheng LIU, Rujira WANOTAYAN, ○Yoshihisa MATSUMOTO

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • Role of XRCC4 C-terminal Part in DNA Double-Strand Break Repair Revealed by Systematically Generated Mutants

    Rujira WANOTAYAN, Mikoto FUKUCHI, Mukesh Kumar SHARMA, Yoshihisa MATSUMOTO

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • Role of DNA-PKs and ATM in the phosphorylation-mediated regulation of XRCC4 International conference

    Shoji Imamichi, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    29th RBC-NIRS International Symposium  2013.11 

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    Venue:Kyoto (Coop Inn Kyoto)  

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  • マウスを用いたDNA二重鎖切断修復能の年齢依存性の検討

    大川 あおい, 松本 義久, 柿沼 志津子, 今岡達彦, 島田義也

    日本原子力学会2014年春の大会  2014.3 

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    Venue:東京都市大学世田谷キャンパス  

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  • adiosensitization of Human Cells by DNA Ligase IV C-Terminus Ectopic Expression

    Liu S, Liu X, Wanotayan R, Sharma MK, Yokoya A, Matsumoto Y

    第20回癌治療増感研究会  2014.6 

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    Venue:高知県民文化ホール  

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  • Functional Study of C-Terminal Region of XRCC4 Protein in DNA Double-Strand Break Repair through Non-Homologous End Joining Pathway

    Wanotayan R, Fukuchi M, Kumar MK, Matsumoto Y

    第20回癌治療増感研究会  2014.6 

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    Venue:高知県民文化ホール  

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  • DNA二重鎖切断修復におけるXRCC4のリン酸化制御へのDNA-PK及ひATM阻害剤の影響

    今道祥二, 松本義久, シャルマ ムケシュクマール

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • Mechanisms of the Recognition and Repair of DNA Double-Strand Breaks And Possible Application in Cancer Therapy International conference

    Yoshihisa Matsumoto

    The Fourth International Symposium on Innovative Nuclear Energy Systems  2013.11 

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    Venue:Tokyo Institute of Technology  

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  • Visualization of the role of NHEJ inhibition in response to ionizing radiation in HeLa Fucci cells International conference

    Rujira Wanotayan, Sicheng Liu, Yoshihisa Matsumoto, Akinari Yokoya

    29th RBC-NIRS International Symposium  2013.11 

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    Venue:Kyoto (Coop Inn Kyoto)  

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  • C-terminal region of DNA ligase IV drives XRCC4/DNA ligase IV complex to chromatin International conference

    Sicheng Liu, Xyunyue Liu, Radhika Pankaj Kamdar, Rujira Wanotayan, Mukesh Kumar Sharma, Noritaka Adachi, Yoshihisa Matsumoto

    29th RBC-NIRS International Symposium  2013.11 

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    Venue:Kyoto (Coop Inn Kyoto)  

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  • Visualization of cell cycle arrest by X-irradiation and NHEJ inhibitors on Hela-Fucci cells

    Sicheng Liu, Rujira Wanotayan, Yoshihisa Matsumoto, Akinari Yokoya

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • XRCC4: The Genuine Target of DNA-PK in Non Homologous End Joining International conference

    Mukesh Kumar Sharma, Radhika Pankaj Kamdar, Shoji Imamichi, Mikoto Fukuchi, Sicheng Liu, Wanotayan Rujira, Yoshihisa Matsumoto

    3rd Asian Congress of Radiation Research  2013.5 

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    Venue:Beijing International Convention Center  

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  • 放射線影響に関する市民対話から見えてきた教育の課題

    田内 広, 松本 英樹, 宇佐美 徳子, 松本 義久, 三谷 啓志, 渡邉 正己

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • カスパーセによるXRCC4切断とXRCC4によるCADの核内移行促進機構の解明

    砂谷優実, カムダル ラディカ パンカジ, シャルマ ムケシュ クマール, 松井 理, 逆井 良, 橋本光正, 松本義久, 岩淵邦芳

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • 福島第一原発事故以来浮彫になった放射線生物学の課題

    松本義久

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • 週齢の異なるマウスにおけるDNA二重鎖切断修復関連タンパク質の発現

    大川あおい, 柿沼志津子, 今岡達彦, 島田 義也, 松本 義久

    日本放射線影響学会第56回大会  2013.10 

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    Venue:クラウンパレス青森  

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  • Identification of phosphorylation sites in XRCC4 mediating its functional regulation by DNA-PK

    Mukesh Kumar Sharma, Radhika Pankaj Kamdar, Shoji Imamichi, Mikoto Fukuchi, Sicheng Liu, Wanotayan Rujira, Yoshihisa Matsumoto

    第19回癌治療増感研究会  2013.6 

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    Venue:東京医科歯科大学  

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  • Creation and analyses of systematic series of XRCC4 mutants

    Wanotayan, R, Fukuchi, M, Sharma, M.K, Matsumoto, Y

    第19回癌治療増感研究会  2013.6 

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    Venue:東京医科歯科大学  

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  • DNA-PKによる内在性XRCC4リン酸化の検出

    Mukesh Kumar Sharma, 今道祥二, 松本義久

    第51 回日本放射線腫瘍学会生物部会学術大会  2013.7 

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    Venue:東北大学艮陵会館  

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  • 原子力合意形成学に関する一考察(?):低線量影響に対するリスクコミュニケーション:先行研究調査

    山野直樹, 安田仲宏, 泉佳伸, 松本義久, 林崎規託, 篠田佳彦

    日本原子力学会2013年秋の大会  2013.9 

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    Venue:八戸工業大学  

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  • ヒト細胞のDNA損傷応答におけるヒストンシャペロンAnti-silencing function 1の機能の解析

    山崎 あかね, 島田 幹男, 松本 義久

    2017年度生命科学系学会合同年次大会  2017.12 

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    Venue:神戸ポートピア  

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  • Molecular mechanisms involved in the repair of DNA double-strand breaks in cells exposed to low-dose-rate γ-radiation Invited International conference

    Tomita, M, Kobayashi, J, Iwabuchi, K, Matsumoto, Y, Adachi, N, Takata, M, Otsuka, K, Sakai, K, Utsumi, H

    3rd International Symposium of RIRBM, Hiroshima University  2013.2 

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    Venue:Hiroshima University  

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  • Identification of phosphorylation sites in XRCC4 mediating its functional regulation by DNA-PK International conference

    Mukesh Kumar Sharma, Yoshihisa Matsumoto

    3rd Asian Congress of Radiation Research  2013.5 

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    Venue:Beijing International Convention Center  

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  • VUV-CDを用いたXRCC4タンパク質の活性化二次構造解析

    西久保 開, 泉 雄大, 藤井 健太郎, 松尾 光一, 松本 義久, 横谷 明徳

    量子生命科学研究会第2回学術集会  2018.5 

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:東京大学弥生講堂一条ホール  

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  • 癌治療増感研究への次のインスピレーション〜シン・ゴジラの放射線感受性〜 Invited

    松本 義久

    第24回癌治療増感研究会  2018.5 

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    Venue:雲仙温泉東園  

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  • Generation of keratinocytes from human induced pluripotent stem cells and analysis of its DNA damage response

    Tomoko Miyake, Mikio Shimada, Yoshihisa Matsumoto, Akitoshi Okino

    The 16th Stem Cell Research Symposium  2018.6 

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    Venue:九州大学医学部  

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  • The role of DNA repair machinery and cell death in induced pluripotent stem cells

    Mikio Shimada, Yoshihisa Matsumoto

    The 16th Stem Cell Research Symposium  2018.6 

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    Venue:九州大学医学部  

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  • DNA修復因子PNKPの機能解析とBRCA1/2変異との合成致死における感受性の検討

    加瀬 直也, 島田 幹男, 中野 洋文, 中村 浩之, 松本 義久

    2017年度生命科学系学会合同年次大会  2017.12 

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    Language:English  

    Venue:神戸ポートピア  

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  • ヒト細胞内におけるGFP-p53融合タンパク質を利用したDNA損傷応答可視化システム

    塚田 海馬, 島田 幹男, 松本 義久

    2017年度生命科学系学会合同年次大会  2017.12 

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    Venue:神戸ポートピア  

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  • 温熱と放射線の併用効果の分子メカニズム〜現状と課題. 第20回菅原・大西記念癌治療増感シンポジウムin奈良

    松本 義久, 山口 基貴, 島田 幹男

    第20回菅原・大西記念癌治療増感シンポジウムin奈良  2018.2 

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    Venue:奈良県文化会館  

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  • DNA二重鎖切断修復欠損細胞の低線量率放射線に対する感受性の解析

    土屋 尚代, 島田 幹男, 小林 純也, 松本 義久

    日本放射線腫瘍学会第56回生物部会学術大会  2018.7 

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    Venue:国立がん研究センター中央病院  

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  • DNA損傷応答タンパク質の活性化スイッチングとエピジェネティック構造変化の研究

    長谷川 真保, 西久保 開, 松本 義久, 藤原 悟, 横谷 明徳

    平成30年度若手放射線生物学研究会専門研究会  2018.9 

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    Venue:麻生大学  

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  • iPS細胞における遺伝子発現変動と放射線照射による細胞死への影響

    島田 幹男, 塚田 海馬, 香川 望, 松本 義久

    平成30年度若手放射線生物学研究会専門研究会  2018.9 

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    Venue:麻生大学  

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  • マウスにおけるDNA二重鎖切断修復タンパク質DNA-PKcs及びXLFの発現の年齢及び組織依存性

    大川 あおい, 柿沼 志津子, 今岡 達彦, 島田 義也, 松本 義久

    日本放射線影響学会第57回大会  2014.10 

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    Venue:かごしま県民交流センター  

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  • BLM遺伝子が調節するDNA損傷修復機構

    Kaima Tsukada, Carl Morrow, Mikio Shimada, Yoshihisa Matsumoto, Andrew N Blackford

    第56回アイソトープ・放射線研究発表会  2019.7  日本アイソトープ協会

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    Venue:東京大学弥生講堂  

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  • 全長トリXRCC4遺伝子の同定と解析

    谷田部 成一郎, 松本 義久

    日本放射線腫瘍学会生物部会第52回生物部会学術大会  2014.7 

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    Venue:メルパルク京都  

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  • Functional Analysis of Disease-associated XRCC4 Mutations and its implication in DNA Repair and Immune System International conference

    Anie Day Asa De Castro, Rujira Wanotayan, Mikio Shimada, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    International Congress of Radiation Resarch 2019  2019.8 

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    Venue:Manchester Central (Manchester, UK)  

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  • 原子力合意形成学に関する一考察(?):低線量影響に関するリスクコミュニケーション:平成25年度活動結果と現状報告

    山野 直樹, 泉 佳伸, 安田 仲宏, 松本 義久, 林崎 規託, 篠田 佳彦

    日本原子力学会2014年秋の大会  2014.9 

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    Venue:京都大学吉田キャンパス  

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  • Phosphorylation of XRCC4 by DNA-dependent protein kinase in DNA double-strand break repair through non-homologous end joining International conference

    Mukesh Kumar SHARMA, Ali Reza AMIRI MOGHANI, Shoji IMAMICHI, Mikoto FUKUCHI, Mikio SHIMADA, Yoshihisa MATSUMOTO

    International Congress of Radiation Resarch 2019  2019.8 

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    Venue:Manchester Central (Manchester, UK)  

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  • DNA損傷によって誘発されるXRCC4のリン酸化とDNA-PKcs、ATMの相補的役割

    松本 義久

    第73回日本癌学会学術総会  2014.9 

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    Venue:パシフィコ横浜  

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  • Analysis of mechanism of DNA repair machinery and cell death in induced pluripotent stem cells International conference

    Mikio Shimada, Kaima Tsukada, Nozomi Kagawa, Yoshihisa Matsumoto

    International Congress of Radiation Resarch 2019  2019.8 

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    Venue:Manchester Central (Manchester, UK)  

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  • 低線量率γ線連続照射下における非相同末端結合の重要性とその意義

    冨田 雅典, 小林 純也, 松本 義久, 内海 博司

    日本放射線影響学会第57回大会  2014.10 

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    Venue:かごしま県民交流センター  

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  • Functional analysis of XRCC4 mutations associated with microcephaly and growth defects International conference

    Anie Day Asa DC, Rujira Wanotayan, Mikio Shimada, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    The 2nd International Symposium on Radiation Therapeutics and Biology & The 34th Radiation Biology Center International Symposium  2018.11 

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    Venue:Kyoto University  

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  • Involvement of DNA-PK Phosphorylation Sites in XRCC4 in the Functional Regulation of Non-Homologous End Joining Repair Pathway

    Sharma MK, Imamichi S, Fukuchi M, Kamdar RP, Liu S, Wanotayan R, Matsumoto Y

    第20回癌治療増感研究会  2014.6 

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    Venue:高知県民文化ホール  

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  • DNA damage-induced phosphorylation of XRCC4 on Ser260 and Ser320 by DNA-PK International conference

    Ali Reza Amiri Moghani, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    3R&3C Symposium  2018.11 

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    Venue:Kanazawa Bunka Hall  

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  • 放射線生物学研究者から見た福島第一原発事故 Invited

    松本 義久

    第27回イオン交換セミナー  2014.7 

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    Venue:上智大学  

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  • 東工大における原子力規制人材育成プログラム「原子力安全・核セキュリティ・保障措置教育の体系化と実践」(2) 2018年度実施状況

    江幡 修一郎, 韓 治暎, 相楽 洋, 松本 義久, 千葉 敏, 林崎 規託, 池上 雅子, 尾本 彰, 竹下 健二, 片渕 竜也, 木倉 宏成, 鷹尾 康一朗

    第 39 回日本核物質管理学会年次大会  2018.11 

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    Venue:東京大学  

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  • XRCC4リジン-アルギニン置換体の作製と解析

    福地 命, Sharma Mukesh Kumar, Wanotayan Rujira, 松本 義久

    日本放射線腫瘍学会生物部会第52回生物部会学術大会  2014.7 

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    Venue:メルパルク京都  

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  • 「シン・ゴジラ」から癌放射線治療へ

    松本 義久

    第15回前立腺癌密封小線源永久挿入治療研究会  2019.1 

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  • DNA二重鎖切断修復におけるXRCC4のリン酸化による制御

    松本 義久, Sharma Mukesh Kumar, 今道 祥二

    日本放射線腫瘍学会生物部会第52回生物部会学術大会  2014.7 

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    Venue:メルパルク京都  

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  • Targeting DNA Ligase IV C-terminus for Radiosensitization

    Sicheng Liu, Rujira Wanotayan, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    日本放射線影響学会第57回大会  2014.10 

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    Venue:かごしま県民交流センター  

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  • Functional studies of XRCC4 C-terminal mutants

    Rujira Wanotayan, Mikoto Fukuchi, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    日本放射線影響学会第57回大会  2014.10 

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    Venue:かごしま県民交流センター  

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  • DNA 損傷・修復の視点から見た低線量率放射線影響

    松本 義久

    日本放射線影響学会第61回大会  2018.11 

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    Venue:長崎ブリックホール  

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  • XRCC4 タンパク質の擬似リン酸化による構造変化の解析

    西久保 開, 長谷川 真保, 泉 雄大, 藤井 健太郎, 松尾 光一, 松本 義久, 横谷 明徳

    日本放射線影響学会第61回大会  2018.11 

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    Venue:長崎ブリックホール  

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  • iPS 細胞における放射線照射による遺伝子発現制御と細胞死への影響

    島田 幹男, 塚田 海馬, 香川 望, 松本 義久

    日本放射線影響学会第61回大会  2018.11 

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    Venue:長崎ブリックホール  

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  • ヒト人工多能性幹細胞における放射線照射後の DNA 損傷応答とアポトーシスの解析

    土屋 尚代, 塚田 海馬, 香川 望, 島田 幹男, 松本 義久

    日本放射線影響学会第61回大会  2018.11 

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    Venue:長崎ブリックホール  

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  • In cellulo phosphorylation of DNA double-strand break repair protein XRCC4 on Ser260 by DNA-PK

    Ali Reza Amiri Moghani, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    日本放射線影響学会第61回大会  2018.11 

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    Venue:長崎ブリックホール  

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  • iPS細胞における放射線照射後のDNA損傷応答に関与するリン酸化・脱リン酸化機構解析

    香川 望, 塚田 海馬, 土屋 尚代, 今村 力也, 島田 幹男, 松本 義久

    平成30年度若手放射線生物学研究会専門研究会  2018.9 

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    Venue:麻生大学  

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  • Regulation of DNA double-strand break repair via non-homologous end joining pathway Invited International conference

    Yoshihisa Matsumoto

    International Workshop on Influence of electromagnetic radiation on human beings, and problems of understandin  2018.9 

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    Venue:Yerevan State University  

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  • GFP-p53を用いたマウスES細胞におけるDNA可視化解析の試み

    古賀 匠, 塚田 海馬, 島田 幹男, 松本 義久, 田川 陽一

    第91回日本生化学会大会  2018.9 

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    Venue:国立京都国際会館  

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  • Effects of hyperthermia on DNA double-strand break repair machineries underlying hyperthermic radiosensitization

    松本 義久, 島田 幹男

    第77回日本癌学会学術総会  2018.9 

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    Venue:大阪国際会議場・リーガロイヤルホテル大阪  

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  • iPS 細胞におけるゲノム安定性維持に関わるリン酸化・脱リン酸化機構解析

    香川 望, 塚田 海馬, 島田 幹男, 松本 義久

    日本放射線影響学会第61回大会  2018.11 

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    Venue:長崎ブリックホール  

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  • Functional Analysis of Disease-associated XRCC4 Mutations and Its Implication in the Development of Immune and Neural Systems

    Anie Day Asa De Castro, Rujira Wanotayan, Mukesh Kumar Sharma, Mikio Shimada, Yoshihisa Matsumoto

    日本放射線影響学会第61回大会  2018.11 

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    Venue:長崎ブリックホール  

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  • Mechanisms of the repair of DNA double-strand breaks Invited International conference

    Yoshihisa Matsumoto

    YITP & YIPQS Workshop Biological & Medical Science based on Physics  2015.11 

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    Venue:Kyoto University Yukawa Memorial Center  

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  • DNA修復蛋白質XRCC4のカスパーゼ依存性切断によるスプライシング調節を介したアポトーシスの促進

    砂谷 優実, Radhika Pankaj Kamdar, Mukesh Kumar Sharma, 松井 理, 逆井 良, 橋本 光正, 松本 義久, 岩淵 邦芳

    BMB2015(第38回日本分子生物学会年会、第88回日本生化学会大会 合同大会)  2015.12 

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    Venue:神戸国際会議場  

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  • 低線量率γ線連続照射下における非相同末端結合の重要性

    冨田 雅典, 小林 純也, 大塚 健介, 松本 義久, 内海 博司

    BMB2015(第38回日本分子生物学会年会、第88回日本生化学会大会 合同大会)  2015.12 

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    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:神戸国際会議場  

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  • Regulation of XRCC4/DNA Ligase IV Complex in DNA Double-strand Break Repair International conference

    Yoshihisa Matsumoto, Mikoto Fukuchi, Sicheng Liu, Shoji Imamichi, Mukesh K Sharma

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • 原子力合意形成学に関する一考察(IX);低線量影響に対するリスクコミュニケーション:低線量影響ガイドブックと実装ガイダンス

    山野 直樹, 泉 佳伸, 安田 仲宏, 篠田 佳彦, 松本 義久, 林崎 規託

    日本原子力学会2015年秋の大会  2015.9 

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    Venue:静岡大学  

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  • グローバル原子力安全・セキュリティ・エージェント養成 (4)高度国際教養科目群

    松本 義久, 齊藤 正樹, 井頭 政之

    日本原子力学会2015年秋の大会  2015.9 

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    Venue:静岡大学  

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  • Recognition and Repair of DNA Double-strand Breaks _ Molecular Mechanisms and Implication in Medicine Invited International conference

    Yoshihisa Matsumoto

    International Workshop on Ionizing and Non-ionizing Radiation Influence on Structure and Biophysical Properties of Living Cells  2015.9 

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    Venue:Tsughkadzor, Armenia (Hotel Russia)  

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  • Differential Expression of Non-homologous End Joining Proteins in the Brain of Young and Adult Mice International conference

    Aoi Okawa, Shizuko Kakinuma, Tatsuhiko Imaoka, Yoshiya Shimada, Yoshihisa Matsumoto

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • Chromatin-binding and Phosphorylation of XRCC4 and XLF Proteins in Response to Ionizing Radiation and DNA Damaging Agent Zeocin International conference

    Ali Reza Amiri Moghani, Mukesh K Sharma, Yoshihisa Matsumoto

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • XRCC4 Phosphorylation By DNA-PK Essential for DNA Double-strand Break Repair International conference

    Mukesh K Sharma, Shoji Imamichi, Mikoto Fukuchi, Radhika P Kamdar, Scheng Liu, Rujira Wanotayan, Yoshihisa Matsumoto

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • Essential Role of Extremely C-terminal Region of XRCC4 Protein in DNA Double-strand Break Repair International conference

    Rujira Wanotayan, Mikoto Fukuchi, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • XRCC4 Overexpression Predicts Poor Prognosis of Patients with Esophageal Squamous Cell Carcinoma Treated with Radiation Therapy International conference

    Kohichi Sakata, Masakazu Hori, Masanori Someya, Kensei Nakata, Tadashi Hasegawa, Yoshihisa Matsumoto

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • Scanning Mutation Analysis of Conserved Lysine Residues in XRCC4 International conference

    Mikoto Fukuchi, Mukesh Kumar Sharma, Rujira Wanotayan, Reiko Watanabe, Shoji Imamichi, Sicheng Liu, Shin-ichiro Kanno, Teruya Nakamura, Akira Yasui, Yoshihisa Matsumoto

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • DNA二重鎖切断の認識・修復の分子機構からがん診断・治療へ Invited

    松本 義久

    第33回法政大学イオンビーム工学研究所シンポジウム  2014.12 

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    Venue:法政大学  

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  • XRCC4 phosphorylation as indicator of DNA-dependent protein kinase functionality in living cells

    Ravindra Mahadeo Samartha, Mukesh Kumar Sharma, Shoji Imamichi, Mikoto Fukuchi, Yoshihisa Matsumoto

    第17回癌治療増感研究シンポジウム  2015.2 

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    Venue:奈良県文化会館  

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  • Asparagine 326 in the extremely C-terminal region of XRCC4 is essential for the cell survival after irradiation International conference

    Rujira Wanotayan, Mikoto Fukuchi, Shoji Imamichi, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    The 30th RBC-NIRS Intenational Symposium- Frontier Radiation Biology  2015.2 

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    Venue:Coop Inn Kyoto (Kyoto, Japan)  

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  • 原子力合意形成学に関する一考察(?):低線量影響に対するリスクコミュニケーション:平成26年度活動成果と現状報告

    山野 直樹, 泉 佳伸, 安田 仲宏, 松本 義久, 林崎 規託, 篠田 佳彦

    日本原子力学会2015年春の年会  2015.3 

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    Venue:茨城大学日立キャンパス  

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  • XRCC4リジン―アルギニン置換体の解析

    福地 命, クマール シャルマ ムケシュ, ワノタヤーン ルジラー, 松本 義久

    日本放射線影響学会第57回大会  2014.10 

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    Venue:かごしま県民交流センター  

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  • DNA二重鎖切断修復におけるDNA-PKのリン酸化の意義:XRCC4リン酸化部位の同定と解析

    松本 義久

    日本放射線影響学会第57回大会  2014.10 

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    Venue:かごしま県民交流センター  

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  • Function of XRCC4 C-terminal Region in DNA Double-Strand Break Repair International conference

    Wanotayan R, Sharma MK, Matsumoto Y

    American Nuclear Society Winter 2014  2014.11 

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    Venue:Anaheim CA, USA  

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  • How do cell find and repair DNA double-strand breaks? _ Molecular biology, cancer therapy and radioprotection Invited International conference

    Matsumoto Y

    7th Thailand-Japan International Academic Conference 2014  2014.11 

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    Venue:University of Tokyo  

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  • Phosphorylation-mediated Regulation of Apoptosis By NHEJ-protein XRCC4 International conference

    Yumi Sunatani, Mukesh Kumar Sharma, Radhika Pankaj Kamdar, Tadashi Matsui, Ryo Sakasai, Mitsumasa Hashimoto, Yoshihisa Matsumoto, Kuniyoshi Iwabuchi

    15th International Congress of Radiation Research  2015.5 

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    Venue:Kyoto International Conference Center  

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  • DNA二重鎖切断修復遺伝子欠損細胞(ヒト細胞)の作製と解析

    松宮 雅典, 松本 義久, 島田 幹男

    日本放射線影響学会第59回大会  2016.10 

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    Venue:JMSアステールプラザ(広島)  

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  • DNA damage-induced phosphorylation of XRCC4 at multiple sites

    Ali Reza Amiri Moghani, Rujira Wanotayan, Mukesh Kumar Sharma, Anie Day Asa De Castro, 島田 幹男, 松本 義久

    日本放射線影響学会第59回大会  2016.10 

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    Venue:JMSアステールプラザ(広島)  

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  • 低線量(率)放射線の生物影響研究の今後に向けて

    松本 義久

    日本放射線影響学会第59回大会  2016.10 

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    Venue:JMSアステールプラザ(広島)  

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  • Ionizing radiation induce genome instability through centrosome overduplication and ciliogenesis International conference

    Mikio Shimada, Hisayo Tsuchiya, Yoshihisa Matsumoto

    The Fifth International Symposium on Innovative Nuclear Energy Systems  2016.10 

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    Venue:Tokyo Institute of Technology  

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  • DNA double strand break repair function of XRCC4 mutants associated with microcephaly and growth defect

    Anie Day Asa De Castro, 松本 義久, 島田 幹男

    日本放射線影響学会第59回大会  2016.10 

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    Venue:JMSアステールプラザ(広島)  

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  • 放射線と温熱の併用処理時のDNA損傷応答メカニズムの解析

    山口 基貴, 松本 義久, 島田 幹男

    日本放射線影響学会第59回大会  2016.10 

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    Venue:JMSアステールプラザ(広島)  

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  • 低線量率放射線応答におけるDNA二重鎖切断修復タンパク質の役割

    土屋 尚代, 島田 幹男, 小林 純也, 松本 義久

    日本放射線影響学会第59回大会  2016.10 

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    Venue:JMSアステールプラザ(広島)  

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  • 低線量放射線の影響ーDNA損傷、疫学データから考える Invited

    松本 義久

    低線量放射線とその影響に関するシンポジウム  2016.9 

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    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:核融合科学研究所  

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  • DNA修復酵素PNKPのゲノム安定性維持における役割

    島田 幹男, 松本 義久

    第89回日本生化学会大会  2016.9 

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    Venue:仙台国際センター  

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  • DNA double strand break repair function of XRCC4 mutants associated with microcephaly and growth defect International conference

    Anie Day Asa De Castro, Rujira Wanotayan, Mikio Shimada, Yoshihisa Matsumoto

    62nd Annual International Meeting Radiation Research Society  2016.10 

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    Venue:Big Island (Hawaii), USA  

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  • 低線量(率)放射線の生物影響における課題

    冨田 雅典, 松本 義久, 小林 純也, 大塚 健介, 藤通 有希, 岩崎 利泰

    日本放射線影響学会第59回大会  2016.10 

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    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:JMSアステールプラザ(広島)  

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  • Fukushima Daiichi Nuclear Power Plant Accident 2011 from the Aspect of Radiation Biology Invited International conference

    Yoshihisa Matsumoto

    ISTC Project A-2089 Workshop  2016.6 

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    Venue:Yerevan State University  

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  • 放射線影響科学から見た低線量放射線の健康リスク

    松本 義久

    日本保健物理学会第49回研究発表会  2016.6 

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    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:弘前文化センター  

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  • がん治療における温熱と放射線の併用効果の分子メカニズム解析

    山口 基貴, 島田 幹男, 松本 義久

    若手放射線生物学研究会平成28年度専門研究会  2016.9 

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    Venue:東京工業大学  

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  • Single Cell Elemental Analysis of Human Cells Using Droplet Injection ICP-AES/MS International conference

    Shunsuke Hosoda, Satoshi Kohno, Mari Aida, Ken Kakegawa, Tomoko Miyake, Takahiro Iwai, Hidekadzu Miyahara, Mikio Shimada, Yoshihisa Matsumoto, Akitoshi Okino

    The 43rd Annual North American Meeting of the Federation of Analytical Chemistry and Spectroscopy Societies (FACSS)  2016.9 

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    Venue:Hyatt Regency Hotel (Minneapolis, MN, USA)  

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  • 話題提供:癌になりやすい組織となりにくい組織―分裂回数か、環境か、遺伝的要因か?

    松本 義久

    第9回Quantum Medicine研究会  2016.3 

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    Venue:茨城大学  

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  • DNA二重鎖切断の認識・修復の分子機構 Invited

    松本 義久

    アイソトープ薬学研究会  2016.3 

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    Venue:横浜ベイホテル東急  

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  • DNA二重鎖切断の認識・修復の分子機構と癌治療・放射線防護 Invited

    松本 義久

    フロンティア研究センター&大学院医歯薬学研究部保健科学部門講演会  2016.5 

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    Venue:徳島大学  

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  • DNA依存性プロテインキナーゼ(DNA-PK)の機能と放射線感受性の予測・制御

    松本 義久

    BMB2015(第38回日本分子生物学会年会、第88回日本生化学会大会 合同大会)  2015.12 

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    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:神戸国際会議場  

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  • DNA二重鎖切断の認識と修復のタンパク質翻訳後修飾による統御 Invited

    松本 義久

    JAEA第1050回金曜セミナー  2015.12 

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    Venue:いばらき量子ビームセンター  

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  • DNA二重鎖切断修復タンパク質XRCC4の点変異体の系統的作製と機能解析

    福地 命, Rujira Wanotayan, Mukesh Kumar Sharma, 今道 祥二, 松本 義久

    第18回癌治療増感研究シンポジウム  2016.2 

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    Venue:奈良県文化会館  

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  • 放射線によるDNA損傷と修復 Invited

    松本 義久

    第6回放射線生物学セミナー  2016.2 

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    Venue:名古屋市立大学医学部  

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  • オラパリブとカンプトテシン併用による放射線増感作用

    三浦 勝利, 坂田 耕一, 染谷 正則, 松本 義久, 松本 英樹, 高橋 昭久, 高木 克, 堀 正和, 中田 健生, 晴山 雅人

    日本放射線腫瘍学会第25回学術大会  2012.11 

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    Venue:東京国際フォーラム  

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  • Analysis of components in CO2 plasma bubbled-up water International conference

    Tomoko Miyake, Hiroaki Kawano, Jyumpei Hosoda, Mikio Shimada, Hidekazu Miyahara, Koichiro Takao, Yosihisa Matsumoto, Akitoshi Okino

    23rd International Symposium on Plasma Chemistry  2017.7 

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    Venue:McGill University (Montr_al, Canada)  

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  • 放射線生物学研究者から見た放射線のリスク Invited

    松本 義久

    第21回漬物技術研究セミナー  2012.3 

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    Venue:東京(江東区森下文化センター)  

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  • シンクロトロン放射を用いたCDスペクトル測定によるDNA修復タンパク質XRCC4の構造解析

    西久保 開, 泉 雄大, 藤井 健太郎, 松本 義久, 横谷 明徳

    若手放射線生物学研究会主催平成29年度専門研究会  2017.9 

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    Venue:東京大学アイソトープ総合センター  

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  • Biological effect of radicals and ultraviolet rays in various gas atmospheric plasmas International conference

    Takamatsu T, Oshita T, Sasaki R, Miyahara H, Matsumoto Y, Okino A

    2012 MRS Spring Meeting and Exhibition  2012.4 

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    Venue:San Francisco (USA)  

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  • ヒト細胞におけるヒストンシャペロンAsf1のDNA損傷応答の解析

    山崎 あかね, 島田 幹男, 松本 義久

    若手放射線生物学研究会主催平成29年度専門研究会  2017.9 

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    Venue:東京大学アイソトープ総合センター  

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  • Plasma gas temperature effect on survival ratio of human cells International conference

    Takamatsu T, Oshita T, Sasaki R, Nakashima N, Miyahara H, Matsumoto Y, Okino A

    4th International Conference on Plasma Medicine  2012.6 

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    Venue:Orl_ans, France  

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  • DNA修復因子Polynucleotide kinase phosphatase (PNKP)の機能解析と抗がん剤開発への応用

    加瀬 直也, 島田 幹男, 松本 義久

    若手放射線生物学研究会主催平成29年度専門研究会  2017.9 

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    Venue:東京大学アイソトープ総合センター  

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  • ギメラシルによる放射線増感効果の検討

    染谷 正則, 高木 克, 坂田 耕一, 晴山 雅人, 松本 義久, 田内 広, 福島 正和

    第47回日本医学放射線学会生物部会学術大会  2012.6 

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    Venue:高知(ホテル日航高知旭ロイヤル)  

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  • シン・ゴジラの放射線感受性

    松本 義久

    第23回癌治療増感研究会  2017.7 

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    Venue:軽井沢プリンスホテルウエスト  

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  • DNA二重鎖切断修復欠損細胞の低線量率放射線に対する感受性

    土屋 尚代, 島田 幹男, 小林 純也, 松本 義久

    第23回癌治療増感研究会  2017.7 

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    Venue:軽井沢プリンスホテルウエスト  

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  • DNA二重鎖切断修復機構のアナトミーと医療応用への展望 Invited

    松本 義久

    第5回 Quantum Medicine研究会  2012.3 

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    Venue:茨城大学理学部  

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  • Structural analysis of DNA repair protein (XRCC4) applying circular dichroism at synchrotron VUV beamline International conference

    Kai Nishikubo, Yudai Izumi, Kentaro Fujii, Yoshihisa Matsumoto, Akinari Yokoya

    1st QST International Symposium Quantum Life Science  2017.7 

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    Venue:Tokyo Bay Makuhari Hall  

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  • 放射線のリスクをどう捉えるべきか Invited

    松本 義久

    第13回ナレッジプール講演会  2012.3 

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    Venue:政策研究大学院大学  

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  • 低線量・低線量率放射線の健康影響 Invited

    松本 義久

    第14回癌治療増感研究シンポジウム公開講座  2012.2 

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    Venue:奈良(猿沢荘)  

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  • ドロプレットICP-MSを用いた単一ヒト細胞の質量分析

    河野 聡史, 相田 真里, 岩井 貴弘, 宮原 秀一, 千葉 光一, 沖野 晃俊, 三宅 智子, 島田 幹男, 松本 義久

    第77回分析化学討論会  2017.5 

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    Venue:龍谷大学深草学舎(京都)  

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  • DNA 損傷応答におけるリン酸化脱リン酸化酵素PNKP の機能解析

    島田 幹男, 加瀬 直也, 塚田 海馬, 松本 義久

    平成29年度日本生化学会関東支部例会  2017.6 

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    Venue:東京医科歯科大学  

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  • 小型線形加速器によるBNCT 照射システムの開発

    日本原子力学会 2010年春の年会  2010 

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  • ヒト細胞でのGFP-p53 融合タンパク質の発現とDNA 損傷応答の解析

    塚田 海馬, 島田 幹男, 松本 義久

    平成29年度日本生化学会関東支部例会  2017.6 

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    Venue:東京医科歯科大学  

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  • Development of BNCT Irradiation System using Compact Linac

    2010 Annual Meeting of the Atomic Energy Society of Japan  2010 

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  • Measurement of reactive oxygen species in plasma bubbled-up water affecting human cultured cells International conference

    Jyumpei Hosoda, Tomoko Miyake, Hiroaki Kawano, Mikio Shimada, Yuriko Matsumura, Hidekazu Miyahara, Atsuo Iwasawa, Yoshihisa Matsumoto, Akitoshi Okino

    The International Conference on Phenomena in Ionized Gases (ICPIG) 2017  2017.7 

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    Venue:Estoril Congress Centre (Estoril, Portugal)  

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  • 放射線の人体への影響 Invited

    松本 義久

    日本保全学会第12回保全セミナー  2012.1 

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    Venue:東京大学  

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  • High-sensitive Elemental Analysis of Single Human Cell using Droplet Injection ICP-AES/MS International conference

    Takahiro Iwai, Shunsuke Hosoda, Satoshi Kohno, Mari Aida, Ken Kakegawa, Tomoko Miyake, Hidekadzu Miyahara, Yoshihisa Matsumoto, Koichi Chiba, Akitoshi Okino

    European Winter Conference on Plasma Spectrochemistry 2017  2017.2 

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    Venue:St. Anton Am Arlberg  

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  • DNA and protein repair to be explored by structural biology Invited International conference

    Yoshihisa Matsumoto

    Hiroshima International Workshop on Circular Dichroism Spectroscopy 2017  2017.2 

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    Venue:Hiroshima Synchrotron Radiation Center  

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  • A Live Cell DNA Damage Response Indicator System Based On p53 Regulation Mechanism

    塚田 海馬, 島田 幹男, 松本 義久

    第56回日本生体医工学会  2017.5 

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    Venue:東北大学  

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  • ドロプレット試料導入ICP-MS/AESを用いた単一ヒト細胞内元素の含有比率測定

    河野 聡史, 相田 真里, 岩井 貴弘, 宮原 秀一, 千葉 光一, 沖野 晃俊, 三宅 智子, 島田 幹男, 松本 義久

    平成29年度日本分光学会年次講演会  2017.5 

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    Venue:早稲田大学  

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  • DNA二重鎖切断の非相同末端結合の新展開と癌治療増感

    松本 義久

    第19回癌治療増感研究シンポジウム  2017.2 

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    Venue:奈良県文化会館  

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  • The role of DNA repair factor Polynucleotide kinase/phosphatase (PNKP) in DNA replication International conference

    Naoya Kase, Mikio Shimada, Yoshihisa Matsumoto

    The 7th International Society of Radiation Neurobiology Conference  2017.2 

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    Venue:Yuzawa  

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  • プラズマバブル水がヒト培養細胞へ及ぼす影響の評価

    細田 順平, 三宅 智子, 島田 幹男, 宮原 秀一, 松本 義久, 沖野 晃俊

    プラズマ核融合学会第33回年次大会  2016.11 

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    Venue:東北大学青葉山キャンパス  

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  • DNA damage-induced phosphorylation of XRCC4 and its role in DNA double-strand break repair International conference

    Ali Reza Amiri Moghani, Rujira Wanotayan, Mukesh Kumar Sharma, Anie Day Asa De Castro, Mikio Shimada, Yoshihisa Matsumoto

    The Fifth International Symposium on Innovative Nuclear Energy Systems  2016.10 

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    Venue:Tokyo Institute of Technology  

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  • XRCC4: target of phosphorylation by DNA-PK in DNA double-strand break repair International conference

    Mukesh Kumar Sharma, Shoji Imamichi, Mikoto Fukuchi, Ali Reza Amiri Moghani, Rujira Wanotayan, Mikio Shimada, Yoshihisa Matsumoto

    10th 3R International Symposium  2016.11 

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    Venue:Hotel Ichibata (Matsue)  

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  • グローバル原子力安全・セキュリティ・エージェント養成(2)放射性物質環境動態

    韓 治暎, 永井 晴康, 竹下 健二, 松本 義久, 相楽 洋

    第37回核物質管理学会日本支部年次大会  2016.11 

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    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:東京工業大学  

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  • グローバル原子力安全・セキュリティ・エージェント養成(1)環境放射線計測フィールドワーク

    松本 義久, 井頭 政之, 小栗 慶之, 千葉 敏, 韓 治暎, 相楽 洋

    第37回核物質管理学会日本支部年次大会  2016.11 

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    Venue:東京工業大学  

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  • Intracellular calcium analysis of single human cell using droplet injection ICP-OES/MS International conference

    Satoshi Kohno, Mari Aida, Tomoko Miyake, Takahiro Iwai, Hidekazu Miyahara, Mikio Shimada, Yoshihisa Matsumoto, Takashi Aoi, Koichi Chiba, Akitoshi Okino

    7th Asia-Pacific Winter Conference on Plasma Spectrochemistry  2017.11 

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    Venue:Kunibiki Messe (Matsue)  

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  • Function of histone chaperone Anti-silencing function 1 (Asf1) in DNA damage response of human cells International conference

    Akane Yamasaki, Mikio Shimada, Yoshihisa Matsumoto

    33rd International Symposium of Radiation Biology Center,Kyoto University  2017.12 

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    Venue:Co-op Inn Kyoto (Kyoto)  

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  • Regulation of non-homologous end joining repair mechanism of DNA double-strand break by kinase activity of DNA-PK International conference

    Sharma, M.K, Matsumoto, Y

    28th RBC-NIRS International Symposium  2012.11 

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    Venue:Kyoto (Coop-Inn Kyoto)  

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  • In situ visualization system for DNA damage response in human cells based on p53 regulation mechanism International conference

    Kaima Tsukada, Mikio Shimada, Yoshihisa Matsumoto

    33rd International Symposium of Radiation Biology Center,Kyoto University  2017.12 

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    Venue:Co-op Inn Kyoto (Kyoto)  

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  • Mechanism of apoptosis induction via regulation of ASAP complex by XRCC4

    砂谷 優実, Radhika Pankaj KAMDAR, Mukesh Kumar SHARMA, 松井 理, 橋本 光正, 松本 義久, 岩淵 邦芳

    第35回日本分子生物学会年会  2012.12 

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:福岡国際会議場  

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  • The functional analysis of DNA repair factor PNKP and susceptibility to synthetic lethality of BRCA 1/2 mutation International conference

    Naoya Kase, Mikio Shimada, Hirofumi Nakano, Hiroyuki Nakamura, Yoshihisa Matsumoto

    33rd International Symposium of Radiation Biology Center,Kyoto University  2017.12 

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    Language:English   Presentation type:Poster presentation  

    Venue:Co-op Inn Kyoto (Kyoto)  

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  • Functional analyses of systematic series of XRCC4 mutants in DNA double-strand break repair

    Wanotayan, R, Sharma, M.K, Matsumoto, Y

    第15回癌治療増感研究シンポジウム  2013.2 

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:猿沢荘(奈良)  

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  • Characterization of XRCC4 Ser260 and Ser320 phosphorylation by DNA-PK International conference

    Ali Reza Amiri Moghani, Mukesh Kumar Sharma, Yoshihisa Matsumoto

    33rd International Symposium of Radiation Biology Center,Kyoto University  2017.12 

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    Language:English   Presentation type:Poster presentation  

    Venue:Co-op Inn Kyoto (Kyoto)  

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  • Importance of DNA-PK phosphorylation in NHEJ repair and cancer radiotherapy

    Sharma, M.K, Matsumoto, Y

    第15回癌治療増感研究シンポジウム  2013.2 

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:猿沢荘(奈良)  

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  • Development of Droplet Injection ICP-AES/MS and Elemental Analysis of Single Human Cancer/Osteosarcoma Cell Invited International conference

    Akitoshi Okino, Satoshi Kohno, Mari Aida, Tomoko Miyake, Takahiro Iwai, Hidekazu Miyahara, Mikio Shimada, Yoshihisa Matsumoto, Takashi Aoi, Koichi Chiba

    7th Asia-Pacific Winter Conference on Plasma Spectrochemistry  2017.11 

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    Language:English   Presentation type:Oral presentation (keynote)  

    Venue:Kunibiki Messe (Matsue)  

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Works

  • DNA二重鎖切断の認識・修復の分子機構に基づく放射線感受性予測・制御の新戦略体系(文部科学省科学研究費補助金 若手研究(A))

    2005 - 2007

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    Work type:Artistic work  

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  • 長期的視点に立ったアジア地域の放射線科学研究基盤強化のための若手研究者の連携(日本学術振興会科学研究費補助金 基盤研究(C))

    2005

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  • Joinasome:DNA二重鎖切断修復に関わる超高次複合体の解明(日本学術振興会科学研究費補助金 萌芽研究)

    2005

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  • DNA二重鎖切断修復酵素を指標とした放射線感受性予測システムの可能性(がん研究振興財団研究奨励助成)

    2004

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    Work type:Artistic work  

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  • DNA二重鎖切断センサーDNA-PKを指標とした新しい放射線感受性・癌罹患性予測法の開発

    2004

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  • DNA二重鎖切断修復の分子機構に基づく新しい抗癌剤・放射線増感剤の開発(原口記念癌研究助成基金)

    2004

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    Work type:Artistic work  

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  • DNA二重鎖切断修復酵素を指標とした放射線感受性予測システムの構築(佐藤記念癌研究助成基金)

    2004

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    Work type:Artistic work  

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  • DNA-PKを介した放射線損傷シグナル伝達機構の解析と癌放射線治療への応用の試み(文部科学省科学研究費補助金 特定領域研究[公募])

    2004

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  • DNA-PKとRB1CC1の協調によるDNA損傷時の細胞生存とがん化抑制機構の解明(がんに関わる特定領域研究 若手支援委員会共同研究支援)

    2004

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  • DNA-PKを介した放射線損傷シグナル伝達機構の解析と癌放射線治療への応用の試み(文部科学省科学研究費補助金 特定領域研究[公募])

    2003

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    Work type:Artistic work  

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  • DNA-PKを介した放射線損傷シグナル伝達機構の解析と癌放射線治療への応用の試み(文部科学省科学研究費補助金 特定領域研究[公募])

    2002

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  • WRN/DNA-PK間相互作用のDNA修復とゲノム安定性維持における意義(がんに関わる特定領域研究(C)若手支援委員会共同研究支援)

    2001

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  • DNA依存性プロテインキナーゼの放射線応答における役割についての研究(財団法人放射線影響協会研究奨励助成)

    2001

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    Work type:Artistic work  

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  • DNA依存性プロテインキナーゼの放射線応答における役割(文部科学省科学研究費補助金 特定領域研究(C)[公募])

    2001

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  • DNA依存性プロテインキナーゼからのアプローチによるがん温熱療法の基礎研究(文部科学省科学研究費補助金 奨励研究(A))

    1999 - 2000

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    Work type:Artistic work  

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  • DNA依存性プロテインキナーゼの性質と放射線応答における役割(文部科学省科学研究費補助金 特別研究員奨励費)

    1996 - 1997

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    Work type:Artistic work  

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Awards

  • JRRS Award

    2024.9   Japanese Radiation Research Society  

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  • IASCT Award

    2020.6   International Association for Sensitization of Cancer Treatment   Molecular Mechanism of DNA Double-strand Break Repair and Application to Cancer Therapy

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  • Excellent Presentation Award in 23rd Research Workshop

    2017.7   International Association for Sensitization of Cancer Treatment   Radiosensitivity of Shin-Godzilla

    MATSUMOTO Yoshihisa

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  • Commendation of Excellent Reviewer

    2014.11   Japan Society for the Promotion of Science  

    MATSUMOTO Yoshihisa

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  • Japanese Group of Radiation Biology Award

    2014.7   Japanese Society for Radiation Oncology, Japanese Group of Radiation Biology  

    MATSUMOTO Yoshihisa

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  • Commendation of Excellent Reviewer

    2012.11   Japan Society for the Promotion of Science  

    MATSUMOTO Yoshihisa

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  • Young Investigator Award in Basic Strategic Research Initiative in Nuclear Power

    2011.2   Basic Strategic Research Initiative in Nuclear Power   Study on the initial stage of the recognition and repair of DNA double-strand breaks

    MATSUMOTO Yoshihisa

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  • Tokyo Tech Award for Challenging Research

    2007.10   Tokyo Institute of Technology   The molecular mechanisms of the recognition and repair of DNA double-strand breaks and its application in cancer radiotherapy

    MATSUMOTO Yoshihisa

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  • Japanese Radiation Research Society Young Investigator Award

    2005.11   Japanese Radiation Research Society   Study on the properties and functions of DNA double-strand break sensor molecule DNA-PK

    Yoshihisa Matsumoto

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    Country:Japan

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Research Projects

  • High-throughput and precision analysis of biological effects of low-dose-rate radiation.

    Grant number:24H00752  2024.4 - 2029.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)

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    Grant amount:\47450000 ( Direct Cost: \36500000 、 Indirect Cost:\10950000 )

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  • Development of ultra-sensitive high-throughput single cell elemental analysis system and creation of single cell metallomics

    Grant number:22H04973  2022.4 - 2027.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (S)

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    Grant amount:\196560000 ( Direct Cost: \151200000 、 Indirect Cost:\45360000 )

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  • Development of a high-sensitive, high-throughput single-cell elemental analysis system directly connected to a flow cytometer

    Grant number:22H00323  2022.4 - 2025.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)

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    Grant amount:\43420000 ( Direct Cost: \33400000 、 Indirect Cost:\10020000 )

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  • Paradigm shift in mutation research brought by next generation sequencing: from specific locus test to whole genome analysis

    Grant number:21K19842  2021.7 - 2023.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Research (Exploratory)

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    Grant amount:\6500000 ( Direct Cost: \5000000 、 Indirect Cost:\1500000 )

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  • The new strategy for radioresistance in cancer associated with p53 mutation using targeted alpha therapy

    Grant number:20H03633  2020.4 - 2024.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

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    Grant amount:\17290000 ( Direct Cost: \13300000 、 Indirect Cost:\3990000 )

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  • Biological Significance of DNA-PK in the Orchestration of Cellular Response to DNA Double-strand Breaks

    Grant number:20H04334  2020.4 - 2023.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

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    Grant amount:\17810000 ( Direct Cost: \13700000 、 Indirect Cost:\4110000 )

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  • 長期的視点に立った放射線に関する科学リテラシー涵養とリスクコミュニケーション人材育成のための小中学校における「目で見る」放射線科学教育の実践研究

    2020.4

    環境省  放射線の健康影響に関する研究調査事業 

    松本義久

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  • p53ライフサイクルを利用して多様な生物でのDNA損傷応答を生きた状態で『見る』

    2017.10 - 2018.3

    文部科学省  英知を結集した原子力科学技術・人材育成推進事業 

    松本 義久

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    Authorship:Principal investigator  Grant type:Competitive

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  • Structural Biology on the Effect of Hyperhtermia on Ku - From DNA Damage Repair to Protein Damage Repair

    2017.4 - 2019.3

    Japan Society for the Promotion of Science  Grant-in-Aid for Challenging Research (Sprouting) 

    MATSUMOTO Yoshihisa

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  • Unification of effects of radiation and chemical substance and evaluation of personal variance in sensitivity

    2016.4 - 2019.3

    Ministry of Environment  Research on Health Effects of Radiation 

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  • The Biological Significance of "Protein Phosphorylating" Function of DNA-PK in DNA Double-strand Break Repair

    2015.4 - 2019.3

    Japan Society for the Promotion of Science  Grant-in-Aid for Scientific Research (B) 

    MATSUMOTO Yoshihisa

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  • Construction of Community-Based Risk Communication Method for Health Effects on Low-Dose Ionizing Radiation

    Grant number:25420902  2013.4 - 2016.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Yamano Naoki, IZUMI Yoshinobu, YASUDA Nakahiro, HAYASHIZAKI Noriyosu, MATSUMOTO Yoshihisa, SHINODA Yoshihiko

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    Grant amount:\5200000 ( Direct Cost: \4000000 、 Indirect Cost:\1200000 )

    A new community-based risk communication method regarding health effects of low-dose ionizing radiation after the Fukushima nuclear accident was constructed. The practical model of the community participatory risk communication approach that takes advantage of the properties of the local government and local communities has been constructed considering scientific evidence of the low-dose radiation exposure, the uncertainty which cannot be verified by science, and the psychological and social impact.
    A social implementation guidance which includes the practical implementation technique together with effective participation of various actors was developed and verified its effectiveness through a social experiment that was intended for Tsuruga city of Fukui Prefecture where is in the vicinity of many nuclear power stations.

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  • Molecular Mechanisms for "Triaging" DNA Double-strand Breaks

    2013.4 - 2015.3

    Japan Society for the Promotion of Science  Grant-in-Aid for Challenging Sprouting Research 

    MATSUMOTO Yoshihisa

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  • Generation of Radiosensitizer by New Strategy Based on the Molecular Mechanisms of DNA Double-strand Break Repair

    2012.4 - 2016.3

    Japan Society for the Promotion of Science  Grant-in-Aid for Scientific Research (B) 

    MATSUMOTO Yoshihisa

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  • ELUCIDATION OF DNA DAMAGE RECOGNITION/REPAIR MECHANISM AND ITS APPLICATION TO CANCER THERAPY

    2012.4 - 2015.3

    Tokyo Biochemical Research Foundation  Grant for Interanational Research Collaboratiion 

    MATSUMOTO Yoshihisa

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  • Systematic Strategy for the Prediction and Control of Radiosensitivity Based on the Life Cycle and Homeostasis of DNA Repair Machinery

    2009.4 - 2012.3

    Ministry of Education, Culture, Sports, Science and Technology  Grant-in-Aid for Young Scientists (A) 

    MATSUMOTO Yoshihisa

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  • Basic Principle for the Biological Action of Hyperthermia Explored by DNA Double-strand Break Sensing Protein Ku

    2009.4 - 2010.3

    Japan Society for the Promotion of Science  Grant-in-Aid for Challenging Sprouting Research 

    MATSUMOTO Yoshihisa

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  • Molecular Mechanisms for the Recognition and Repair of DNA Double-strand Breaks and Its Application to Cancer Radiotherapy

    2008.12 - 2010.11

    Japan Society for the Promotion of Science  Research Fund for JSPS International Postdoctral Resarch Fellow 

    MATSUMOTO Yoshihisa

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  • DNA二重鎖切断の認識・修復の初期過程に関する研究

    2008.10 - 2010.3

    文部科学省  原子力基礎基盤戦略研究イニシアティブ 若手原子力プログラム 

    松本 義久

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  • Radiation sensitization though regulation of transcriptional factor Sp1

    Grant number:18390330  2006 - 2009

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    HOSOI Yoshio, MATSUMOTO Yoshihisa, ENOMOTO Atsushi

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    Grant amount:\18500000 ( Direct Cost: \15200000 、 Indirect Cost:\3300000 )

    The protein and mRNA levels of Sp1, Ku70, Ku80, DNA-PKcs, XRCC4, NBS1, MRE11 and MDC1 were down regulated by the Sp1-siRNA treatment. The DSBs-repair after 80 Gy irradiation and DNA-PK activity were suppressed by the Spl-siRNA treatment. The surviving fraction after irradiation was also suppressed by the Spl-siRNA treatment.

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  • 子宮頚がん発生におけるHPV DNAの組み込みとE6、E7発現増加機構の解明

    Grant number:18012051  2006 - 2007

    日本学術振興会  科学研究費助成事業  特定領域研究

    清野 透, 齋藤 真子, 温川 恭至, 松本 義久

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    Grant amount:\11400000 ( Direct Cost: \11400000 )

    不死化子宮頸部由来正常細胞株にHPV16ゲノムを導入することで数10-100コピーのHPV16ゲノムをepisomalに維持する細胞株の樹立に成功した.この細胞は従来報告されているものと異なり,feeder細胞なしに長期間維持出来ることが明らかになった.子宮頸部異形成由来の細胞株W12などと異なり,これまでHPVゲノムの細胞ゲノムへの組み込みは確認されていない.この細胞株を用いることで,episomal HPV16ゲノムの維持と組み込み機構ならびに,がん化の引き金になるE6とE7遺伝子の高発現に至る機構の解析が再現性良くできると考えている.この細胞でDNA-PKcs,Ku70,Ku86など非相同組み換え修復に関わる遺伝子発現をノックダウンした.これまでのところ,組み込み頻度への影響は確認出来ていないが,Ku70,Ku86をそれぞれ単独でノックダウンするとKu70,Ku86の両者の蛋白量が減少しDNA-PKcs蛋白量も減少する傾向が見られた.<BR> DNA-PK活性と子宮頸癌との相関は,統計学的に確かであるが,原因が分からずその解明は非常に重要である.DNA-PK活性の個人差が出てくる理由の追及を進め,DNA-PKcs,Ku86,Ku70の発現調節にE2Fファミリーが制御に関わっている可能性を見出した.具体的には,8名(がん患者4名,健常者4名)のリンパ球のマクロアレイ解析を行い,DNA-PK活性やサブユニット発現と相関が強い分子を探索した.その結果,Rap1B,Rad9,XRCC3,SUMO,E2F1,Cyclin D1などの発現が正の相関を示し,逆に,強い逆相関を示したものとしてRbp130が見いだされた.このことから,E2Fファミリーが調節に関わっている可能性を考えられたが,実際,DNA-PKcs,Ku86,Ku70全てのプロモータ領域にE2Fのbinding siteが見つかり,PHAで刺激するとDNA-PK活性とともに,mRNA発現上昇も見られた.更にこれを検証するためには,siRNAなどを用いた実験を進めている.また,E2F以外の転写調節機構が関わる可能性も検討していく必要がある。

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  • A New Sistematic Strategy for the Prediction and Control of Radiosensitivity Based on the Molecular Mechanisms for the Recognition and Repair of DNA double-strand Breaks

    2005.4 - 2008.3

    Ministry of Education, Culture, Sports, Science and Technology  Grant-in-Aid for Young Scientists (A) 

    MATSUMOTO Yoshihisa

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  • Joinasome: Elucidation of Super-high Order Molecular Complex for DNA Double-strand Break Repair

    2005.4 - 2006.3

    Japan Society for the Promotion of Science  Grant-in-Aid for Sprouting Scientific Research 

    MATSUMOTO Yoshihisa

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  • Building the Network of Young Radiation Scientists in Asia for Reinforcement of Radiation Science

    2005.4 - 2006.3

    Japan Society for the Promotion of Science  Grant-in-Aid for Scientific Research (C) 

    MATSUMOTO Yoshihisa

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  • DNA二重鎖切断センサーDNA-PKを指標とした新しい放射線感受性・癌罹患性予測法の開発

    2004.4 - 2005.3

    財団法人大阪癌研究会  一般学術研究助成金 

    松本 義久

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  • DNA二重鎖切断修復酵素を指標とした放射線感受性予測システムの可能性

    2004.4 - 2005.3

    がん研究振興財団  研究奨励助成 

    松本 義久

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  • DNA二重鎖切断修復酵素を指標とした放射線感受性予測システムの構築

    2004.4 - 2005.3

    佐藤記念癌研究助成基金  佐藤記念癌研究助成基金 

    松本 義久

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  • DNA二重鎖切断修復の分子機構に基づく新しい抗癌剤・放射線増感剤の開発

    2004.4 - 2005.3

    原口記念癌研究助成基金  原口記念癌研究助成基金 

    松本 義久

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  • Molecular mechanism of DNA double-strand break repair (especially in vertebrates) II. Components and assembly of DNA end-joining machinery

    2004

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  • Application of DNA double-strand break recognition/repair mechanism I. A new approach for the modulation of radiosensitivity

    2003

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  • Analysis of Signal Transduction Mechanisms via DNA-PK and Its Possible Application to Cancer Radiotherapy

    2002.4 - 2005.3

    Ministry of Education, Culture, Sports, Science and Technology  Grant-in-Aid for Scientific Research in Special Field 

    MATSUMOTO Yoshihisa

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  • 応答特異抗体とDNA arrayによる放射線感受性予測システムの構築

    Grant number:14657211  2002 - 2003

    日本学術振興会  科学研究費助成事業  萌芽研究

    鈴木 紀夫, 森田 明典, 松本 義久, 榎本 敦

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    Grant amount:\3300000 ( Direct Cost: \3300000 )

    放射線感受性予測のためヒトT細胞腫癌由来MOLT-4細胞の放射線照射後のシグナル伝達と遺伝子発現制御機構を解析した。細胞死を放射線感受性の指標に、jnkのドミナントネガティブタンパク発現細胞、もしくは、特異的阻害剤による遺伝子発現の変化を、リン酸化特異的抗体によるWestern解析とRT-PCR, DNA arrayを用いて、検討した。X線照射後、SAPK/JNKリン酸化に続いて、転写因子c-Mycのm RNA、タンパク量の線量依存的・時間依存的減少、c-Myc antisense oligonucleolides導入やc-Myc阻害剤処理によるアポトーシスが誘導過程について、DNA arrayによる遺伝子発現の網羅的解析のデータを裏付けるために、RT-PCRなどいくつかの実験で再検証を行う実験を行った。スポットする遺伝子配列や感度の制御について検討し、DNA arrayの信頼性を向上させることが、放射線応答遺伝子・感受性決定遺伝子DNA array開発や臨床におけるDNA arrayを用いた診断法の確立へつながると考える。
    また放射線照射後に誘導または修飾されるタンパク質に対する新規抗体の開発を目的として、これまでp53のセリン15、37、46のリン酸化特異的抗体、DNA依存性プロテインキナーゼの基質の1つであるXRCC4タンパク質に対するリン酸化特異抗体や我々が発見したアポトーシスの過程で新規に誘導され、p42/SETβのカスパーゼ切断産物であるp41特異的抗体を作製し他の各種細胞で検証してきた。放射線誘発アポトーシスにおいてp54JNKがカスパーゼ3によって切断されて生ずるp52を新たな細胞死マーカータンパクとして加えることができた。

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  • Clarification of response mechanism in U937 cells against heat treatment

    Grant number:14370271  2002 - 2003

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    SUZUKI Norio, MORITA Akinori, ENOMOTO Atsushi, MATSUMOTO Yoshihisa

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    Grant amount:\12800000 ( Direct Cost: \12800000 )

    The overall goal of the present project has been to analyze mechanisms of heat-induced apoptotic cell death and radio-sensitization for better treatment of cancer. Toward this goal, we have accomplished the following progress.
    1)We have clarified the involvement of ceramide-SAP/JNK pathway, and radio-sensitization process in heat-induced apoptotic cell death.
    2)RT-PCR analysis of apoptosis-related genes revealed that the expression of c-myc gene was reduced in the process of cell death. The introduction of c-myc antisense oligonucleotides or the treatment of c-Myc inhibitor induced cell death.
    3)Involvement and the role of DNA-PK in radio-sensitization by heat was evaluated using various repair deficient and knockout mutants of mammalian cells and DT40 chicken cells.
    4)We found appearance of fragment of JNK, which were identified as cleaved products by Caspase 3 from INK.

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  • DNA double-strand break repair enzymes and cancer susceptibility

    2002

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  • DNA依存性プロテインキナーゼの放射線応答における役割についての研究

    2001.4 - 2002.3

    財団法人放射線影響協会  研究奨励助成 

    松本 義久

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  • Role of DNA-dependent Protein Kinase in Radiation Response

    2001.4 - 2002.3

    Ministry of Education, Culture, Sports, Science and Technology  Grant-in-Aid for Scientific Research in Special Field (C) 

    MATSUMOTO Yoshihisa

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  • Inhibition of DNA-PK activity by phosphorothioate oligonucleotides

    Grant number:12470184  2000 - 2002

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    HOSOI Yoshio, MATSUMOTO Yoshihisa, SUZUKI Norio

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    Grant amount:\13100000 ( Direct Cost: \13100000 )

    Phosphorothioate oligonudeotides and suramin bind to heparin binding proteins including DNA polymerases, and inhibit their functions. In the present study, we report inhibition of DNA-dependent protein kinase (DNA-PK) activity by phosphorothioate oiigonucleotides, suramin and heparin. Inhibitory effect of phosphorothioate oligonudeotides on DNA-PK activity was increased with length and reached a plateau at 36-mer. The base composition of phosphorothioate digonucleotides did not affect the inhibitory effect The inhibitory effect by phosphorothioate oligodeoxycytidine 36-mer can be about 200-fold greater than that by the phosphodiester oligodeoxycytidine 36-mer. The inhibitory effect was also observed with purified DNA-PK, which suggests direct interaction between DNA-PK and phosphorothioate oligonucleotides. DNA-PK will have different binding positions for double-stranded DNA and phosphorothioate oligodeoxycytidine 36-mer because they were not competitive in DNA-PK activation. Suramin and heparin inhibited DNA-PK activity with IC_<50> of 1.7 μM and 0.27 μg/ml respectively. DNA-PK activities and DNA double-stranded breaks (DSBs) repair in cultured cells were significantly suppressed by the treatment with suramin in vivo. Our present observations suggest that suramin mav possibly result in sensitization of cells to ionizing radiation bv inactivation of DNA-PK and the impairment of DSBs repair.

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  • Analysis of signal transduction and nuclear denaturation in radiation-induced cell death

    Grant number:12470185  2000 - 2001

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    SUZUKI Norio, HIRANO Kazuya, ENOMOTO Atsushi, MATSUMOTO Yoshihisa

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    Grant amount:\1800000 ( Direct Cost: \1800000 )

    The overall goal of the present project has been to analyze a mechanism of X-ray-induced apoptotic cell death in human T-cell leukemia cell line MOLT-4. Toward this goal, the purpose of the project were 1) to examine the involvement of p53 and/or SAPK/JNK, 2) to identify genes downstream of the p53 or SAPK/JNK, and to analyze the expressions of apoptosis-related genes by quantative RT-PCR methods, 3) to study a role of a new radiation-induced protein p41 in cell death.
    1) To examine the involvement of ceramide-SAPK/JNK pathway, the effect of acid sphingomyelinase inhibitor (D609) on X-ray-induced apoptotic cell death was studied. D609 suppressed X-ray-induced apoptotic cell death as well as phosphorylation of JNK.
    2) RT-PCR analysis of apoptosis-related genes revealed that the expression of c-myc gene was reduced following X-irradiation, but not in an X-ray-resistant variant cell line Rh-1a. The introduction of c-myc antisense oligonucleotides into MOLT-4 cells or the treatment of c-Myc inhibitor induced cell death.
    3) Specific antibodies for p41 and p42 have been generated. Western blot analysis showed that the activation of caspase-9, caspase-7, and caspas-3 ran paralleled with the generation of p41. Especially, caspase-7 among those was considered important in p41 generation.

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  • Basic Research on Cancer Hyperthermia thourgh Approach from DNA-dependent Protein Kinase

    1999.4 - 2001.3

    Ministry of Education, Culture, Sports, Science and Technology  Grant-in-Aid for Encouragement of Young Researchers (A) 

    MATSUMOTO Yoshihisa

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  • 遺伝子発現を利用した照射効果測定

    Grant number:11670870  1999 - 2000

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    平野 和也, 別府 正敏, 鈴木 紀夫, 松本 義久

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    Grant amount:\3500000 ( Direct Cost: \3500000 )

    In vivoでの腫瘍の放射線応答、照射効果の解析を行うため、担がん動物(ヌードマウス)を用いて、これまで確立してきたWestern法、FCM法(血中腫瘍細胞用)をHT29大腸癌細胞のMUC1 mucinの定量に応用した。さらにGFP標識細胞を利用してin vivoでの照射後、少数のGFP標識細胞を回収し、MUC1等の放射線応答遺伝子の発現の変化を解析を行った。
    まずヒト大腸がんHT29細胞。照射装置:X線は当教室の島津製(Pantak)X線発生装置より得られる200kVp,20mAX線を用いた。
    1)GFP標識細胞株の作製。GFP(Green fluorescent proteins)遺伝子ベクターをヒト腫瘍細胞株(HT-29)にトランスフェクトし、蛍光を発するGFP蛋白を安定に発現する細胞株を蛍光顕微鏡、flowcytometerで確認、選択した。
    HT-29/GFP細胞をヌードマウスに移植し、40日後にマウスを全身照射0,6,10,20,30,50Gy照射し、Tumor suspensionを作製し、解析した。その結果、照射後1〜4日まで細胞のMUCl量は生存率の減少に応じて、線量および時間依存的に増加した。またin vivoでの照射後、約8〜10時間にMUC1量の増加が認められた。これによりMUC1のin vitroとin vivoでの応答パターンを比較することが可能となったが、さらに慎重な解析が必要である。さらに他の細胞系、応答分子、測定系について解析をすすめる予定である。本年度は、特定の細胞株、特定の放射線応答分子についてではあるが、in vivoでX線照射した後にGFP標識細胞選択回収し、放射線応答分子の発現を解析する系を確立することができた。以上により、本研究においてMUC1の発現に注目することとした。その結果、in vitroとin vivoで応答に違いのあった遺伝子については、さらにその原因を調べ、in vivoでの照射効果判定への応用の可能性を検討する。

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  • Molecular mechanism of DNA double-strand break repair (especially in vertebrates) I. True substrates of DNA-PK and significance of phosphorylation

    1998

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  • Moleucular mechanism of synergistic effect of hyperthermia and radiation in cancer therapy

    1996

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  • Molecular Properties of DNA-dependent Protein Kinase and Its Role in Radiation Response

    1995.5 - 1998.3

    Ministry of Education, Culture, Sports, Science and Technology  Research Fund for JSPS Predoctoral Resarch Fellow 

    MATSUMOTO Yoshihisa

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  • Application of DNA double-strand break recognition/repair mechanism I. Prediction of radiation response based on the expression, function or activity of DNA double-strand break repair enzymes

    1995

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Teaching Experience

  • Radiation Biology and Medicine

    Institution:Tokyo Institute of Technology

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  • Materials and Molecular Engineering

    2020.11 - 2020.12 Institution:Tokyo Institute of Technology

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  • 生物工学基礎

    2020.7 - 2020.8 Institution:東京工業大学

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  • 環境安全論

    Institution:東京工業大学

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  • 原子核工学基礎第四

    Institution:東京工業大学

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  • Basic Nuclear Engineering IV

    Institution:Tokyo Institute of Technology

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  • 放射線計測フィールドワーク

    Institution:東京工業大学

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  • 放射性物質環境動態

    Institution:東京工業大学

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