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http://purl.uniprot.org/citations/17031492http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17031492http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17031492http://www.w3.org/2000/01/rdf-schema#comment"It has been well established that FADD plays a critical role in the membrane bound death-inducing signaling complexes. Herein, we report that endogenous FADD could interact with ectopic or endogenous RTN3/HAP. ER-bound RTN3 protein recruited endogenous FADD to the ER membrane and subsequently initiated caspase-8 cascade, including activation of caspase-8, processing of Bid and release of cytochrome c from mitochondria. Furthermore, we demonstrated that endogenous FADD was recruited by ER-bound endogenous RTN3 to the ER membrane under the tunicamycin stimulation. The dominant negative form of FADD containing DD could abolish these RTN3 generated events in the caspase-8 cascade. Moreover, we found that RTN3 induced caspase-9 processing was only partially resulted from caspase-8 activation (data unshown), indicating that multiple caspase cascades participated in the apoptosis from RTN3 over-expression. Furthermore, NogoB/ASY, a homologue of RTN3 and a potential RTN3 interacting protein, also associated with FADD and induced cytochrome c release in a FADD dependent manner."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.org/dc/terms/identifier"doi:10.1007/s10495-006-0082-0"xsd:string
http://purl.uniprot.org/citations/17031492http://purl.org/dc/terms/identifier"doi:10.1007/s10495-006-0082-0"xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Dong W."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Dong W."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Qi Y."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Qi Y."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Zhu L."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Zhu L."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Xiang R."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/author"Xiang R."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/name"Apoptosis"xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/name"Apoptosis"xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/pages"1923-1932"xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/pages"1923-1932"xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/title"Adaptor FADD is recruited by RTN3/HAP in ER-bound signaling complexes."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/title"Adaptor FADD is recruited by RTN3/HAP in ER-bound signaling complexes."xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/17031492http://purl.uniprot.org/core/volume"11"xsd:string