2011 Fiscal Year Final Research Report
Analysis of a new mechanism on homology-dependent repair
Project/Area Number |
22710053
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Risk sciences of radiation/Chemicals
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Research Institution | Kyoto University |
Principal Investigator |
KATO Akihiro 京都大学, 放射線生物研究センター, 研究員 (70423051)
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Project Period (FY) |
2010 – 2011
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Keywords | DNA修復 / 相同組換え |
Research Abstract |
In order to clarify the biological significance of the physical interaction between NBS1 and RAD51, we tried to establish a NBS1 mutant that was not able to bind to RAD51. In this process, we found that NBS1 interacted with RAD51 through MRE11. The MRE11 mutant that could not interact with RAD51 had full activity of homology-dependent repair of DNA double-strand breaks(DSBs). Cells expressing the MRE11 mutant did not show sensitivity to ionizing radiation. These results indicate that the interaction between NBS1 and RAD51 does not have an important role in DSB repair but has a role in other mechanisms.
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Research Products
(10 results)
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[Journal Article] NBS1recruits RAD18 viaa RAD6-like do mainand regulates Polη-dependent translesion DNA synthesis2011
Author(s)
Yanagihara H, Kobayashi J, Tateishi S, Kato A, Matsuura S, Tauchi H, Yamada K, Takezawa J, Sugasawa K, Masutani C, Hanaoka F, Weemaes CM, Mori T, Zou L, Komatsu K
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Journal Title
Molecular Cell
Volume: Volume 43
Pages: 788-797
DOI
Peer Reviewed
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[Journal Article] Regulation of homologous recombination by RNF20-dependent H2B ubiquitination2011
Author(s)
Nakamura K, Kato A, Kobayashi J, Yanagihara H, Sakamoto S, Oliveira DV, Shimada M, Tauchi H, Suzuki H, Tashiro S, Zou L, Komatsu K.
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Journal Title
Molecular Cell
Volume: Volume 43
Pages: 515-528
DOI
Peer Reviewed
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