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http://purl.uniprot.org/citations/19706769http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19706769http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19706769http://www.w3.org/2000/01/rdf-schema#comment"The Bcl-2 family of proteins consists of both antiapoptotic and proapoptotic factors, which share sequence homology within conserved regions known as Bcl-2 homology domains. Interactions between Bcl-2 family members, as well as with other proteins, regulate apoptosis through control of mitochondrial membrane permeability and release of cytochrome c. Here we identify a novel regulator of apoptosis that lacks Bcl-2 homology domains but acts by binding Bcl-2 and modulating its antiapoptotic activity. To identify regulators of apoptosis, we performed expression profiling in human primary fibroblasts treated with tumor necrosis factor-alpha (TNF-alpha), a potent inflammatory cytokine that can regulate apoptosis and functions, at least in part, by inducing expression of specific genes through NF-kappaB. We found that the gene undergoing maximal transcriptional induction following TNF-alpha treatment was G(0)-G(1) switch gene 2 (G0S2), the activation of which also required NF-kappaB. We show that G0S2 encodes a mitochondrial protein that specifically interacts with Bcl-2 and promotes apoptosis by preventing the formation of protective Bcl-2/Bax heterodimers. We further show that ectopic expression of G0S2 induces apoptosis in diverse human cancer cell lines in which endogenous G0S2 is normally epigenetically silenced. Our results reveal a novel proapoptotic factor that is induced by TNF-alpha through NF-kappaB and that interacts with and antagonizes Bcl-2."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.org/dc/terms/identifier"doi:10.1158/0008-5472.can-09-0128"xsd:string
http://purl.uniprot.org/citations/19706769http://purl.org/dc/terms/identifier"doi:10.1158/0008-5472.can-09-0128"xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Zhu X."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Zhu X."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Teodoro J.G."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Teodoro J.G."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Green M.R."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Green M.R."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"El-Assaad W."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"El-Assaad W."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Huber W.E."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Huber W.E."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Keys R.A."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Keys R.A."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Santra M.K."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Santra M.K."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Welch C."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/author"Welch C."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/name"Cancer Res."xsd:string
http://purl.uniprot.org/citations/19706769http://purl.uniprot.org/core/name"Cancer Res."xsd:string