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• W3014348148 endingPage "e1008701" @default.
• W3014348148 startingPage "e1008701" @default.
• W3014348148 abstract "FANCJ helicase mutations are known to cause hereditary breast and ovarian cancers as well as bone marrow failure syndrome Fanconi anemia. FANCJ plays an important role in the repair of DNA inter-strand crosslinks and DNA double-strand breaks (DSBs) by homologous recombination (HR). Nonetheless, the molecular mechanism by which FANCJ controls HR mediated DSB repair is obscure. Here, we show that FANCJ promotes DNA end resection by recruiting CtIP to the sites of DSBs. This recruitment of CtIP is dependent on FANCJ K1249 acetylation. Notably, FANCJ acetylation is dependent on FANCJ S990 phosphorylation by CDK. The CDK mediated phosphorylation of FANCJ independently facilitates its interaction with BRCA1 at damaged DNA sites and promotes DNA end resection by CtIP recruitment. Strikingly, mutational studies reveal that ATP binding competent but hydrolysis deficient FANCJ partially supports end resection, indicating that in addition to the scaffolding role of FANCJ in CtIP recruitment, its helicase activity is important for promoting end resection. Together, these data unravel a novel function of FANCJ helicase in DNA end resection and provide mechanistic insights into its role in repairing DSBs by HR and in genome maintenance." @default.
• W3014348148 created "2020-04-10" @default.
• W3014348148 creator A5007013110 @default.
• W3014348148 creator A5049222210 @default.
• W3014348148 date "2020-04-06" @default.
• W3014348148 modified "2023-10-11" @default.
• W3014348148 title "FANCJ helicase promotes DNA end resection by facilitating CtIP recruitment to DNA double-strand breaks" @default.
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• W3014348148 doi "https://doi.org/10.1371/journal.pgen.1008701" @default.
• W3014348148 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7162537" @default.
• W3014348148 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32251466" @default.
• W3014348148 hasPublicationYear "2020" @default.
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