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http://purl.uniprot.org/citations/12447390http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12447390http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12447390http://www.w3.org/2000/01/rdf-schema#comment"Activation of the ataxia telangiectasia mutated (ATM) kinase triggers diverse cellular responses to ionizing radiation (IR), including the initiation of cell cycle checkpoints. Histone H2AX, p53 binding-protein 1 (53BP1) and Chk2 are targets of ATM-mediated phosphorylation, but little is known about their roles in signalling the presence of DNA damage. Here, we show that mice lacking either H2AX or 53BP1, but not Chk2, manifest a G2-M checkpoint defect close to that observed in ATM(-/-) cells after exposure to low, but not high, doses of IR. Moreover, H2AX regulates the ability of 53BP1 to efficiently accumulate into IR-induced foci. We propose that at threshold levels of DNA damage, H2AX-mediated concentration of 53BP1 at double-strand breaks is essential for the amplification of signals that might otherwise be insufficient to prevent entry of damaged cells into mitosis."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.org/dc/terms/identifier"doi:10.1038/ncb884"xsd:string
http://purl.uniprot.org/citations/12447390http://purl.org/dc/terms/identifier"doi:10.1038/ncb884"xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Chen J."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Chen J."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Naka K."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Naka K."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Xia Z."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Xia Z."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Carpenter P.B."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Carpenter P.B."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Bonner W.M."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Bonner W.M."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Chen H.-T."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Chen H.-T."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Camerini-Otero R.D."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Camerini-Otero R.D."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Motoyama N."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Motoyama N."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Nussenzweig A."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Nussenzweig A."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Fernandez-Capetillo O."xsd:string
http://purl.uniprot.org/citations/12447390http://purl.uniprot.org/core/author"Fernandez-Capetillo O."xsd:string