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http://purl.uniprot.org/citations/11342610http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11342610http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11342610http://www.w3.org/2000/01/rdf-schema#comment"Protein kinase C (PKC)-activating phorbol esters protect T cells from Fas-induced apoptosis. However, the mechanism of this protective effect and the identity of the relevant PKC isoform(s) are poorly understood. Here, we show that PKCtheta plays a selective and important role in this protection. Fas triggering led to a selective caspase-3-dependent cleavage of the enzyme and proteasome-mediated degradation and inactivation of its catalytic fragment. These events preceded the onset of apoptosis. Pharmacological inhibition of PKCtheta promoted Fas-mediated apoptosis in three different types of T cells. Conversely, constitutively active PKCtheta (and, to a lesser degree, PKCepsilon) selectively protected T cells from Fas-induced apoptosis. We provide evidence that the distant Bcl-2 family member, BAD, is a PKCtheta substrate, is phosphorylated by TCR stimulation, and can mediate at least in part the anti-apoptotic effect of PKCtheta."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.166.10.5955"xsd:string
http://purl.uniprot.org/citations/11342610http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.166.10.5955"xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/author"Villalba M."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/author"Villalba M."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/author"Altman A."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/author"Altman A."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/author"Bushway P."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/author"Bushway P."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/pages"5955-5963"xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/pages"5955-5963"xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/title"Protein kinase C-theta mediates a selective T cell survival signal via phosphorylation of BAD."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/title"Protein kinase C-theta mediates a selective T cell survival signal via phosphorylation of BAD."xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/volume"166"xsd:string
http://purl.uniprot.org/citations/11342610http://purl.uniprot.org/core/volume"166"xsd:string
http://purl.uniprot.org/citations/11342610http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11342610
http://purl.uniprot.org/citations/11342610http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11342610
http://purl.uniprot.org/citations/11342610http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11342610
http://purl.uniprot.org/citations/11342610http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11342610