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2016 Fiscal Year Final Research Report

Analysis of DNA-damage-tolerance mechanisms that facilitate restart of stalled DNA replication

Research Project

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Project/Area Number 25340030
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Risk sciences of radiation and chemicals
Research InstitutionKyoto 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
KeywordsDNA損傷トレランス / 複製後修復 / 組換え修復 / ユビキチン
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.

Free Research Field

分子生物学

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Published: 2018-03-22  

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