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ATM activation is impaired in human cells defective in RecQL4 helicase activity

DC Field Value Language
dc.contributor.authorPark, Soon-Young-
dc.contributor.authorKim, Hyunsup-
dc.contributor.authorIm, Jun-Sub-
dc.contributor.authorLee, Joon-Kyu-
dc.creator이준규-
dc.date.accessioned2020-01-23T07:25:42Z-
dc.date.available2020-04-05T07:25:42Z-
dc.date.created2019-11-29-
dc.date.created2019-11-29-
dc.date.issued2019-02-
dc.identifier.citationBiochemical and Biophysical Research Communications, Vol.509 No.2, pp.379-383-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://hdl.handle.net/10371/163624-
dc.description.abstractRecQL4 has been shown to be involved in DNA replication and repair, but its role in DNA damage checkpoint pathway has not been reported. Here, we show that RecQL4 plays an important role in the activation of ataxia telangiectasia mutated (ATM)-dependent checkpoint pathway in human cells. Cells depleted with RecQL4 or Rothmund-Thomson syndrome cells showed significant impairment in the activation of ATM and the downstream effector proteins such as checkpoint kinase 2 and p53 after DNA damage. This defect was recovered with the expression of wild type RecQL4 but not any mutant RecQL4 proteins with defective helicase activities. While RecQL4 failed to show any direct interaction with ATM, it stably interacted with the Mre11-Rad50-Nbs1 complex that is essential for the activation of ATM and was localized on the DNA damage foci. Thus, our results suggest that the helicase activity of RecQL4 plays an important role in the activation of ATM-dependent checkpoint pathway against DNA double strand breaks in human cells. (C) 2018 Elsevier Inc. All rights reserved.-
dc.language영어-
dc.language.isoENGen
dc.publisherAcademic Press-
dc.titleATM activation is impaired in human cells defective in RecQL4 helicase activity-
dc.typeArticle-
dc.identifier.doi10.1016/j.bbrc.2018.12.151-
dc.citation.journaltitleBiochemical and Biophysical Research Communications-
dc.identifier.wosid000458094800009-
dc.identifier.scopusid2-s2.0-85058990653-
dc.description.srndOAIID:RECH_ACHV_DSTSH_NO:T201908070-
dc.description.srndRECH_ACHV_FG:RR00200001-
dc.description.srndADJUST_YN:-
dc.description.srndEMP_ID:A075639-
dc.description.srndCITE_RATE:2.705-
dc.description.srndDEPT_NM:생물교육과-
dc.description.srndEMAIL:joonlee@snu.ac.kr-
dc.description.srndSCOPUS_YN:Y-
dc.citation.endpage383-
dc.citation.number2-
dc.citation.startpage379-
dc.citation.volume509-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorLee, Joon-Kyu-
dc.identifier.srndT201908070-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusDNA-
dc.subject.keywordPlusASSOCIATION-
dc.subject.keywordPlusMUTATIONS-
dc.subject.keywordPlusREQUIRES-
dc.subject.keywordPlusREPAIR-
dc.subject.keywordPlusMCM10-
dc.subject.keywordPlusGENE-
dc.subject.keywordAuthorRecQL4-
dc.subject.keywordAuthorATM-
dc.subject.keywordAuthorDNA damage checkpoint pathway-
dc.subject.keywordAuthorDNA double strand break-
dc.subject.keywordAuthorRothmund-Thomson syndrome-
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