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http://purl.uniprot.org/citations/18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18946037http://www.w3.org/2000/01/rdf-schema#comment"Fas-associated death domain protein (FADD) and caspase-8 (casp8) are vital intermediaries in apoptotic signaling induced by tumor necrosis factor family ligands. Paradoxically, lymphocytes lacking FADD or casp8 fail to undergo normal clonal expansion following antigen receptor cross-linking and succumb to caspase-independent cell death upon activation. Here we show that T cells lacking FADD or casp8 activity are subject to hyperactive autophagic signaling and subvert a cellular survival mechanism into a potent death process. T cell autophagy, enhanced by mitogenic signaling, recruits casp8 through interaction with FADD:Atg5-Atg12 complexes. Inhibition of autophagic signaling with 3-methyladenine, dominant-negative Vps34, or Atg7 shRNA rescued T cells expressing a dominant-negative FADD protein. The necroptosis inhibitor Nec-1, which blocks receptor interacting protein kinase 1 (RIP kinase 1), also completely rescued T cells lacking FADD or casp8 activity. Thus, while autophagy is necessary for rapid T cell proliferation, our findings suggest that FADD and casp8 form a feedback loop to limit autophagy and prevent this salvage pathway from inducing RIPK1-dependent necroptotic cell death. Thus, linkage of FADD and casp8 to autophagic signaling intermediates is essential for rapid T cell clonal expansion and may normally serve to promote caspase-dependent apoptosis under hyperautophagic conditions, thereby averting necrosis and inflammation in vivo."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0808597105"xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Morrissette N.S."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Walsh C.M."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Arechiga A.F."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Leverrier S."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Bell B.D."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Weist B.M."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Luhrs K.A."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/author"Newton R.H."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/name"Proc Natl Acad Sci U S A"xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/pages"16677-16682"xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/title"FADD and caspase-8 control the outcome of autophagic signaling in proliferating T cells."xsd:string
http://purl.uniprot.org/citations/18946037http://purl.uniprot.org/core/volume"105"xsd:string
http://purl.uniprot.org/citations/18946037http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18946037
http://purl.uniprot.org/citations/18946037http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18946037
http://purl.uniprot.org/uniprot/#_A0A0A0MQN4-mappedCitation-18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18946037
http://purl.uniprot.org/uniprot/#_A0A087WQT6-mappedCitation-18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18946037
http://purl.uniprot.org/uniprot/#_A0A385JBX3-mappedCitation-18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18946037
http://purl.uniprot.org/uniprot/#_D3YZW7-mappedCitation-18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18946037
http://purl.uniprot.org/uniprot/#_F7D1J2-mappedCitation-18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18946037
http://purl.uniprot.org/uniprot/#_G9M4M6-mappedCitation-18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18946037
http://purl.uniprot.org/uniprot/#_Q4FK85-mappedCitation-18946037http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18946037