| Project/Area Number |
23310041
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Mitsumasa 金沢医科大学, 一般教育機構, 准教授 (70293975)
ISHIGAKI Yasuhito 金沢医科大学, 総合医学研究所, 准教授 (20232275)
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| Co-Investigator(Renkei-kenkyūsha) |
SUNATANI Yumi 金沢医科大学, 医学部, 助教 (70581057)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥20,020,000 (Direct Cost: ¥15,400,000、Indirect Cost: ¥4,620,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2011: ¥14,690,000 (Direct Cost: ¥11,300,000、Indirect Cost: ¥3,390,000)
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| Keywords | アポトーシス / X線照射 / DNA二重鎖切断 / DNA損傷修復 / 53BP1 / p53 / p21 / スタウロスポリン / 修復 / 核 / 分子生物学 / 放射線 |
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| Research Abstract |
p53 binding protein-1 (53BP1) facilitates non-homologous end joining repair of DNA double-strand breaks. In this study, we examined functional interaction between 53BP1 and p53 in apoptotic cells. We found that 53BP1 is cleaved into a fragment of 53BP1 in a caspase-dependent manner. 53BP1 cleavage is observed in both cells with wild-type and mutant p53. Some of the 53BP1 fragments are localized on the surface of apoptotic cells, suggesting a role of 53BP1 in elimination of apoptotic cells by a macrophage. Downregulation of 53BP1 reduces transcription of several p53 target genes. However, binding of p53 on the promoter in these genes is not affected by 53BP1 downregulation, suggesting that 53BP1 regulates transcriptional activity of p53 by regulating modification of p53 on the promoter in the target genes.
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