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http://purl.uniprot.org/citations/16862143http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16862143http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16862143http://www.w3.org/2000/01/rdf-schema#comment"The cellular DNA-damage response is a signaling network that is vigorously activated by cytotoxic DNA lesions, such as double-strand breaks (DSBs). The DSB response is mobilized by the nuclear protein kinase ATM, which modulates this process by phosphorylating key players in these pathways. A long-standing question in this field is whether DSB formation affects chromatin condensation. Here, we show that DSB formation is followed by ATM-dependent chromatin relaxation. ATM's effector in this pathway is the protein KRAB-associated protein (KAP-1, also known as TIF1beta, KRIP-1 or TRIM28), previously known as a corepressor of gene transcription. In response to DSB induction, KAP-1 is phosphorylated in an ATM-dependent manner on Ser 824. KAP-1 is phosphorylated exclusively at the damage sites, from which phosphorylated KAP-1 spreads rapidly throughout the chromatin. Ablation of the phosphorylation site of KAP-1 leads to loss of DSB-induced chromatin decondensation and renders the cells hypersensitive to DSB-inducing agents. Knocking down KAP-1, or mimicking a constitutive phosphorylation of this protein, leads to constitutive chromatin relaxation. These results suggest that chromatin relaxation is a fundamental pathway in the DNA-damage response and identify its primary mediators."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.org/dc/terms/identifier"doi:10.1038/ncb1446"xsd:string
http://purl.uniprot.org/citations/16862143http://purl.org/dc/terms/identifier"doi:10.1038/ncb1446"xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Shiloh Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Shiloh Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Taya Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Taya Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Lukas C."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Lukas C."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Lukas J."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Lukas J."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Bartek J."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Bartek J."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Schultz D.C."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Schultz D.C."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Bekker-Jensen S."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Bekker-Jensen S."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Galanty Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Galanty Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Ziv Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Ziv Y."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Bielopolski D."xsd:string
http://purl.uniprot.org/citations/16862143http://purl.uniprot.org/core/author"Bielopolski D."xsd:string