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http://purl.uniprot.org/citations/11266364http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11266364http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11266364http://www.w3.org/2000/01/rdf-schema#comment"Apoptosis signal-regulating kinase (ASK) 1 is activated in response to various cytotoxic stresses including TNF, Fas and reactive oxygen species (ROS) such as H(2)O(2), and activates c-Jun NH(2)-terminal kinase (JNK) and p38. However, the roles of JNK and p38 signaling pathways during apoptosis have been controversial. Here we show that by deleting ASK1 in mice, TNF- and H(2)O(2)-induced sustained activations of JNK and p38 are lost in ASK1(-/-) embryonic fibroblasts, and that ASK1(-/-) cells are resistant to TNF- and H(2)O(2)-induced apoptosis. TNF-but not Fas-induced apoptosis requires ROS-dependent activation of ASK1-JNK/p38 pathways. Thus, ASK1 is selectively required for TNF- and oxidative stress-induced sustained activations of JNK/p38 and apoptosis."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.org/dc/terms/identifier"doi:10.1093/embo-reports/kve046"xsd:string
http://purl.uniprot.org/citations/11266364http://purl.org/dc/terms/identifier"doi:10.1093/embo-reports/kve046"xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Takahashi T."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Takahashi T."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Takeda K."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Takeda K."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Matsuzawa A."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Matsuzawa A."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Morita K."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Morita K."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Minowa O."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Minowa O."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Noda T."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Noda T."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Ichijo H."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Ichijo H."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Miyazono K."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Miyazono K."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Nishitoh H."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Nishitoh H."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Tobiume K."xsd:string
http://purl.uniprot.org/citations/11266364http://purl.uniprot.org/core/author"Tobiume K."xsd:string