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

Authors
Ha, GH | Ji, JH  | Chae, S | Park, J | Kim, S | Lee, JK | Kim, Y | Min, S  | Park, JM | Kang, TH | Lee, H | Cho, H  | Lee, CW
Citation
Nature communications, 10. : 1577-1577, 2019
Journal Title
Nature communications
ISSN
2041-1723
Abstract
DNA 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.
MeSH

DOI
10.1038/s41467-019-09641-9
PMID
30952868
Appears in Collections:
Journal Papers > Research Organization > Genomic Instability Research Center
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
Ajou Authors
민, 선우  |  조, 혜성  |  지, 재훈
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