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유전체항상성연구단
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ATAD5 promotes replication restart by regulating RAD51 and PCNA in response to replication stress

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dc.contributor.authorSu Hyung Park-
dc.contributor.authorNalae Kang-
dc.contributor.authorSong E.-
dc.contributor.authorWie M.-
dc.contributor.authorEun A. Lee-
dc.contributor.authorSunyoung Hwang-
dc.contributor.authorLee D.-
dc.contributor.authorJae Sun Ra-
dc.contributor.authorIn Bae Park-
dc.contributor.authorJieun Park-
dc.contributor.authorSukhyun Kang-
dc.contributor.authorJun Hong Park-
dc.contributor.authorHohng S.-
dc.contributor.authorKyoo-young Lee-
dc.contributor.authorKyungjae Myung-
dc.date.available2020-01-31T00:50:53Z-
dc.date.created2020-01-07-
dc.date.issued2019-12-
dc.identifier.issn2041-1723-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/6720-
dc.description.abstract© 2019, The Author(s).Maintaining stability of replication forks is important for genomic integrity. However, it is not clear how replisome proteins contribute to fork stability under replication stress. Here, we report that ATAD5, a PCNA unloader, plays multiple functions at stalled forks including promoting its restart. ATAD5 depletion increases genomic instability upon hydroxyurea treatment in cultured cells and mice. ATAD5 recruits RAD51 to stalled forks in an ATR kinase-dependent manner by hydroxyurea-enhanced protein-protein interactions and timely removes PCNA from stalled forks for RAD51 recruitment. Consistent with the role of RAD51 in fork regression, ATAD5 depletion inhibits slowdown of fork progression and native 5-bromo-2ʹ-deoxyuridine signal induced by hydroxyurea. Single-molecule FRET showed that PCNA itself acts as a mechanical barrier to fork regression. Consequently, DNA breaks required for fork restart are reduced by ATAD5 depletion. Collectively, our results suggest an important role of ATAD5 in maintaining genome integrity during replication stress-
dc.description.uri1-
dc.language영어-
dc.publisherNATURE PUBLISHING GROUP-
dc.titleATAD5 promotes replication restart by regulating RAD51 and PCNA in response to replication stress-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000502773900001-
dc.identifier.scopusid2-s2.0-85076601047-
dc.identifier.rimsid70965-
dc.contributor.affiliatedAuthorSu Hyung Park-
dc.contributor.affiliatedAuthorNalae Kang-
dc.contributor.affiliatedAuthorEun A. Lee-
dc.contributor.affiliatedAuthorSunyoung Hwang-
dc.contributor.affiliatedAuthorJae Sun Ra-
dc.contributor.affiliatedAuthorIn Bae Park-
dc.contributor.affiliatedAuthorJieun Park-
dc.contributor.affiliatedAuthorSukhyun Kang-
dc.contributor.affiliatedAuthorJun Hong Park-
dc.contributor.affiliatedAuthorKyoo-young Lee-
dc.contributor.affiliatedAuthorKyungjae Myung-
dc.identifier.doi10.1038/s41467-019-13667-4-
dc.identifier.bibliographicCitationNATURE COMMUNICATIONS, v.10, no.1, pp.5718-
dc.citation.titleNATURE COMMUNICATIONS-
dc.citation.volume10-
dc.citation.number1-
dc.citation.startPage5718-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > 1. Journal Papers (저널논문)
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