2016 Fiscal Year Final Research Report
Molecular mechanisms of crosstalk between DNA-damage response and signal transduction
| Project/Area Number |
25290044
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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 |
Tumor biology
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松本 雅記 九州大学, 生体防御医学研究所, 准教授 (60380531)
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| Co-Investigator(Renkei-kenkyūsha) |
NIIDA Hiroyuki 浜松医科大学, 医学部, 准教授 (20336671)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Keywords | DNA障害応答 / シグナル伝達 / リン酸化 |
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| Outline of Final Research Achievements |
We found that Mig-6, an internal inhibitor of EGFR,is phosphorylated accompanied by EGF stimulation but also UV-irradiation. The results suggest that there is a crosstalk between EGF-signaling and DNA-damage response. Next, we found that HBO1,a histone acetyltransferase, phosphorylated Ser50/Ser53 of HBO1 by ATR after UV irradiation. HBO1 is ubiquitylated by CUL4-DDB1/DDB2 and degraded 6h after UV-irradiation. Moreover, we found that HBO1 participated in nucleotide excision repair(NAR). UV-DNA-damege induced phosphorylation of HBO1 promoted acetylation of histone H3 to induce structural change of chromatin in the damaged sites. These results suggested that the HBO1-mediated chromatin conformational change promoted recruitment of NER-related factors to enhanced the NER.
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| Free Research Field |
分子生物学
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