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Pellino1 regulates reversible ATM activation via NBS1 ubiquitination at DNA double-strand breaks

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dc.contributor.authorHa, GH-
dc.contributor.authorJi, JH-
dc.contributor.authorChae, S-
dc.contributor.authorPark, J-
dc.contributor.authorKim, S-
dc.contributor.authorLee, JK-
dc.contributor.authorKim, Y-
dc.contributor.authorMin, S-
dc.contributor.authorPark, JM-
dc.contributor.authorKang, TH-
dc.contributor.authorLee, H-
dc.contributor.authorCho, H-
dc.contributor.authorLee, CW-
dc.date.accessioned2020-10-21T07:20:14Z-
dc.date.available2020-10-21T07:20:14Z-
dc.date.issued2019-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/18720-
dc.description.abstractDNA double-strand break (DSB) signaling and repair are critical for genome integrity. They rely on highly coordinated processes including posttranslational modifications of proteins. Here we show that Pellino1 (Peli1) is a DSB-responsive ubiquitin ligase required for the accumulation of DNA damage response proteins and efficient homologous recombination (HR) repair. Peli1 is activated by ATM-mediated phosphorylation. It is recruited to DSB sites in ATM- and gammaH2AX-dependent manners. Interaction of Peli1 with phosphorylated histone H2AX enables it to bind to and mediate the formation of K63-linked ubiquitination of NBS1, which subsequently results in feedback activation of ATM and promotes HR repair. Collectively, these results provide a DSB-responsive factor underlying the connection between ATM kinase and DSB-induced ubiquitination.-
dc.language.isoen-
dc.subject.MESHAtaxia Telangiectasia Mutated Proteins-
dc.subject.MESHCell Cycle Proteins-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHDNA Breaks, Double-Stranded-
dc.subject.MESHDNA Repair-
dc.subject.MESHHumans-
dc.subject.MESHNuclear Proteins-
dc.subject.MESHUbiquitin-Protein Ligases-
dc.subject.MESHUbiquitination-
dc.titlePellino1 regulates reversible ATM activation via NBS1 ubiquitination at DNA double-strand breaks-
dc.typeArticle-
dc.identifier.pmid30952868-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6450972/-
dc.contributor.affiliatedAuthor지, 재훈-
dc.contributor.affiliatedAuthor민, 선우-
dc.contributor.affiliatedAuthor조, 혜성-
dc.type.localJournal Papers-
dc.identifier.doi10.1038/s41467-019-09641-9-
dc.citation.titleNature communications-
dc.citation.volume10-
dc.citation.date2019-
dc.citation.startPage1577-
dc.citation.endPage1577-
dc.identifier.bibliographicCitationNature communications, 10. : 1577-1577, 2019-
dc.identifier.eissn2041-1723-
dc.relation.journalidJ020411723-
Appears in Collections:
Journal Papers > Research Organization > Genomic Instability Research Center
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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