2017 Fiscal Year Final Research Report
A DNA damage-independent role for 53BP1 in apoptotic cells
| Project/Area Number |
26281025
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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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 |
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| Co-Investigator(Kenkyū-buntansha) |
逆井 良 金沢医科大学, 医学部, 助教 (10549950)
砂谷 優実 金沢医科大学, 医学部, 講師 (70581057)
石垣 靖人 金沢医科大学, 総合医学研究所, 教授 (20232275)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAMURA Akira 金沢医科大学, 医学部, 教授 (20344723)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | 53BP1 / DNA二重鎖切断 / アポトーシス |
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| Outline of Final Research Achievements |
53BP1 accumulates at sites of DNA double-strand breaks (DSBs), and facilitates non-homologous end joining repair of DSBs. We found that 53BP1 is cleaved into a fragment in a caspase-dependent manner in apoptotic cells. This 53BP1 cleavage was observed in apoptosis induced by not only X-ray irradiation, but also treatment with staurosporine, a non-DNA damaging apoptosis-inducer. Some of the 53BP1 fragments are localized on the surface of apoptotic cells. The surface localization of the 53BP1 fragment was observed in apoptotic cells which lacked expression of RNF8 or RNF168, ubiquitin ligases required for accumulation of 53BP1 at DSB sites. These data suggest that in apoptotic cells, 53BP1 plays a role independent on the role of 53BP1 in DNA damage responses.
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| Free Research Field |
放射線影響科学
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