Analysis of DNA-damage-tolerance mechanisms that facilitate restart of stalled DNA replication
Project/Area Number |
25340030
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Risk sciences of radiation and chemicals
|
Research Institution | Kyoto University |
Principal Investigator |
MOTEGI AKIRA 京都大学, 医学研究科, 助教 (80452332)
|
Co-Investigator(Renkei-kenkyūsha) |
MASUTANI MITSUKO 長崎大学, 大学院医歯薬総合研究科, 教授 (60238904)
|
Project Period (FY) |
2013-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | DNA損傷トレランス / 複製後修復 / 組換え修復 / ユビキチン / 相同組換え / DNA修復 |
Outline of Final Research Achievements |
In this study, we showed that simultaneous genetic disruption of the ubiquitin ligase SHPRH and FANC, one of core factors in the Fanconi Anemia (FA) pathway, substantially rescued hypersensitivity towards cisplatin, an inter-strand cross-linking (ICL) agent. This observation suggests that SHPRH-dependent pathway antagonizes to the FA pathway. We also showed that PARP-1 prohibits resection in in vitro extract assay and that low expression of CtIP nuclease in breast cancer correlates with poor prognosis and hypersensitivity towards PARP inhibitors.
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Report
(5 results)
Research Products
(10 results)