2011 Fiscal Year Final Research Report
Analysis for regulation of RNR activity during DNA damage repair
| Project/Area Number |
21590315
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Hamamatsu University School of Medicine (2010-2011)
Nagoya City University (2009) |
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Principal Investigator |
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| Project Period (FY) |
2009 – 2011
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| Keywords | 細胞医化学 |
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| Research Abstract |
A balanced deoxyribonucleotide(dNTP) supply is essential for DNA repair. Here, we found that ribonucleotide reductase(RNR) subunits RRM1 and RRM2 accumulated very rapidly at damage sites. RRM1 bound physically to Tip60. Chromatin immunoprecipitation analyses of cells with an I-SceI cassette revealed that RRM1 bound to a damage site in a Tip60-dependent manner. Active RRM1 mutants lacking Tip60 binding failed to rescue an impaired DNA repair in RRM1-depleted G1-phase cells. Inhibition of RNR recruitment by an RRM1 C-terminal fragment sensitized cells to DNA damage. We propose that Tip60-dependent recruitment of RNR plays an essential role in dNTP supply for DNA repair.
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[Journal Article] Essential role of Tip60-dependent recruitment of ribonucleotide reductase at DNA damage sites in DNA repair during G1 phase2010
Author(s)
Niida H, Katsuno Y, Sengoku M, Shimada M, Yukawa M, Ikura M, Ikura T, Kohno K, Shima H, Suzuki H, Tashiro S, Nakanishi M
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Journal Title
Genes Dev
Volume: 24
Pages: 333-338
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