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- W2057587611 abstract "Chk1 is a critical effector of DNA damage checkpoints necessary for the maintenance of chromosome integrity during cell cycle progression. Here we report, that Chk1 co-localized with the nucleolar marker, fibrillarin in response to radiation-induced DNA damage in human cells. Interestingly, in vitro studies using GST pull down assays identified the dual-specificity serine/threonine nucleolar phosphatase Cdc14B as a Chk1 substrate. Furthermore, Chk1, but not a kinase-dead Chk1 control, was shown to phosphorylate Cdc14B using an in vitro kinase assay. Co-immunoprecipitation experiments using exogenous Cdc14B transfected into human cells confirmed the interaction of Cdc14B and Chk1 during cell cycle. In addition, reduction of Chk1 levels via siRNA or UCN-01 treatment demonstrated that Chk1 activation following DNA damage was required for Cdc14B export from the nucleolus. These studies have revealed a novel interplay between Chk1 kinase and Cdc14B phosphatase involving radiation-induced nucleolar shuttling to facilitate error-free cell cycle progression and prevent genomic instability." @default.
- W2057587611 created "2016-06-24" @default.
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- W2057587611 date "2011-02-15" @default.
- W2057587611 modified "2023-10-16" @default.
- W2057587611 title "The DNA damage effector Chk1 kinase regulates Cdc14B nucleolar shuttling during cell cycle progression" @default.
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- W2057587611 doi "https://doi.org/10.4161/cc.10.4.14901" @default.
- W2057587611 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3174002" @default.
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- W2057587611 hasPublicationYear "2011" @default.
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