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http://purl.uniprot.org/citations/23871434http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23871434http://www.w3.org/2000/01/rdf-schema#comment"WIP1 (wild-type p53-induced phosphatase 1) functions as a homeostatic regulator of the ataxia telangiectasia mutated (ATM)-mediated signaling pathway in response to ionizing radiation (IR). Here we identify homeodomain-interacting protein kinase 2 (HIPK2) as a protein kinase that targets WIP1 for phosphorylation and proteasomal degradation. In unstressed cells, WIP1 is constitutively phosphorylated by HIPK2 and maintained at a low level by proteasomal degradation. In response to IR, ATM-dependent AMPKα2-mediated HIPK2 phosphorylation promotes inhibition of WIP1 phosphorylation through dissociation of WIP1 from HIPK2, followed by stabilization of WIP1 for termination of the ATM-mediated double-strand break (DSB) signaling cascade. Notably, HIPK2 depletion impairs IR-induced γ-H2AX foci formation, cell-cycle checkpoint activation, and DNA repair signaling, and the survival rate of hipk2+/-mice upon γ-irradiation is markedly reduced compared to wild-type mice. Taken together, HIPK2 plays a critical role in the initiation of DSB repair signaling by controlling WIP1 levels in response to IR."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2013.06.010"xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Choi H.H."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Isono K."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Lee Y."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Lee C."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Koseki H."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Park S.H."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Ahn J.W."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Choi D.W."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Kim S.T."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Kwon S."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Choi C.Y."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Na W."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Kwon Y.K."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Yoo H.Y."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Yeom J."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Yi E."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Seo K.W."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Shin M.K."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/author"Kabir M.H."xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/name"Mol Cell"xsd:string
http://purl.uniprot.org/citations/23871434http://purl.uniprot.org/core/pages"374-385"xsd:string