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• W2404179619 endingPage "790" @default.
• W2404179619 startingPage "782" @default.
• W2404179619 abstract "Previous studies have linked the DNA damage response to mitotic progression machinery. Mitotic kinases, such as Aurora A kinase and Polo‐like kinase, are involved in the phosphorylation of cell cycle regulators in response to DNA damage. Here, we investigated the potential involvement of Aurora A kinase in the activation of the Fanconi anemia ( FA )/ BRCA pathway, which participates in cellular response to DNA interstrand cross‐link lesions ( ICL ). Initially, we detected interactions between Aurora A kinase and FANCA protein, one of the components of the FA nuclear core complex. Silencing of Aurora A kinase led to inhibition of monoubiquitination of FANCD 2 and formation of nuclear foci, the final consequences of FA / BRCA pathway activation upon ICL induction. An in vitro kinase assay revealed that Aurora A kinase phosphorylates S165 of FANCA . Moreover, this phosphorylation event was induced by the treatment with mitomycin C ( MMC ), an ICL ‐inducing agent. In cells overexpressing S165A mutant FANCA , monoubiquitination of FANCD 2 and nuclear foci formation was impaired and cellular sensitivity to MMC was enhanced. These results suggest that S165 phosphorylation by Aurora A kinase is required for proper activation of the FA / BRCA pathway in response to DNA damage." @default.
• W2404179619 created "2016-06-24" @default.
• W2404179619 creator A5000169747 @default.
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• W2404179619 date "2016-06-08" @default.
• W2404179619 modified "2023-10-04" @default.
• W2404179619 title "Aurora A kinase is required for activation of the Fanconi anemia/ <scp>BRCA</scp> pathway upon <scp>DNA</scp> damage" @default.
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• W2404179619 doi "https://doi.org/10.1002/2211-5463.12087" @default.
• W2404179619 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4932458" @default.
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• W2404179619 hasPublicationYear "2016" @default.
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