2017 Fiscal Year Final Research Report
Analysis of the mechanism of cell sensitivity against anti-cancer drug caused by ubiquitination-dependent DNA-PK activation
| Project/Area Number |
15K16127
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Risk sciences of radiation and chemicals
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
SAKASAI Ryo 金沢医科大学, 医学部, 助教 (10549950)
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| Research Collaborator |
SHIBATA Atsushi 群馬大学, 大学院医学系研究科・大学院研究教育支援センター, 研究講師 (30707633)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | DNA二本鎖切断 / 非相同末端連結 / 相同組換え修復 |
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| Outline of Final Research Achievements |
Anti-cancer drug camptothecin (CPT) causes DNA double-strand break (DSB) containing a single-DNA end that is referred to as one-ended DSB. Given that contribution of non-homologous end joining (NHEJ) to the repair of one-ended DSBs are considered to sensitize cells to CPT, it is important to reveal the mechanism of NHEJ contribution to the repair of one-ended DSBs for consideration of CPT efficacy in the chemotherapy.
Several researches suggested that UbcH5 is involved in the appearance of chromosome aberrations and CPT-resistance via NHEJ. SIAH1 was also identified as E3 ubiquitin ligase that is involved in NHEJ activation, but it has showed different phenotypes from UbcH5 so far.
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| Free Research Field |
分子生物学
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