Project/Area Number |
25870534
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Functional biochemistry
Molecular biology
|
Research Institution | Nagasaki University |
Principal Investigator |
GUO Chaowan 長崎大学, 原爆後障害医療研究所, 客員研究員 (70645283)
|
Project Period (FY) |
2013-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | ヌクレオチド除去修復 / 紫外線高感受性症候群 / UVSSA / RNAポリメラーゼII / ユビキチン化 / ヌクレオチド除去修復機構 / TC-NER / コケイン症候群 / DNA修復 |
Outline of Final Research Achievements |
Transcription-Coupled Nucleotide Excision Repair (TC-NER) resolving the transcription-blocking DNA damages from our genome. Defective in TC-NER causes two genetic diseases, Cockayne syndrome (CS) and UV-sensitive syndrome (UVSS). CS patients usually exhibit photosensitivity, neurological degeneration and severe developmental defects, while UVSS patients are only sensitive to sunlight and display mild clinical features. In previous study, Nakazawa et al. identified the UVSSA gene as the responsible gene of UVSS, which encoded a novel TC-NER factor UVSSA that interacts with TC-NER machinery and stabilizes the CS complex. UVSSA also facilitates ubiquitination of RNA polymerase IIo that stalled at DNA damage sites. Recent reports shown that the ubiquitination may involve in regulation of TC-NER, thus we aimed to uncover the roles of UVSSA in RNA polymerase IIo ubiquitination during the initiation step of TC-NER, then provide more insights into the processing of stalled RNA polymerase.
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