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http://purl.uniprot.org/citations/19088195http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19088195http://www.w3.org/2000/01/rdf-schema#comment"The transcription factor E2F-1 drives proliferation and death, but the mechanisms that differentially regulate these divergent actions are poorly understood. The hypoxia-inducible death factor Bnip3 is an E2F-1 target gene and integral component of the intrinsic mitochondrial death pathway. The mechanisms that govern Bnip3 gene activity remain cryptic. Herein we show that the transcription factor NF-kappaB provides a molecular switch that determines whether E2F-1 signals proliferation or death under physiological conditions. We show under basal nonapoptotic conditions that NF-kappaB constitutively occupies and transcriptionally silences Bnip3 gene transcription by competing with E2F-1 for Bnip3 promoter binding. Conversely, in the absence of NF-kappaB, or during hypoxia when NF-kappaB abundance is reduced, basal Bnip3 gene transcription is activated by the unrestricted binding of E2F-1 to the Bnip3 promoter. Genetic knock-down of E2F-1 or retinoblastoma gene product over-expression in cardiac and human pancreatic cancer cells deficient for NF-kappaB signaling abrogated basal and hypoxia-inducible Bnip3 transcription. The survival kinase PI3K/Akt inhibited Bnip3 expression levels in cells in a manner dependent upon NF-kappaB activation. Hence, by way of example, we show that the transcriptional inhibition of E2F-1-dependent Bnip3 expression by NF-kappaB highlights a survival pathway that overrides the E2F-1 tumor suppressor program. Our data may explain more fundamentally how cells, by selectively inhibiting E2F-1-dependent death gene transcription, avert apoptosis down-stream of the retinoblastoma/E2F-1 cell cycle pathway."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0807735105"xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Zhang T."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Shaw J."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Yurkova N."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Aguilar F."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Gang H."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Kirshenbaum L.A."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Weidman D."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Scramstad C."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/author"Weisman H."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/name"Proc Natl Acad Sci U S A"xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/pages"20734-20739"xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/title"Antagonism of E2F-1 regulated Bnip3 transcription by NF-kappaB is essential for basal cell survival."xsd:string
http://purl.uniprot.org/citations/19088195http://purl.uniprot.org/core/volume"105"xsd:string
http://purl.uniprot.org/citations/19088195http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19088195
http://purl.uniprot.org/citations/19088195http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19088195
http://purl.uniprot.org/uniprot/O09139#attribution-8BEA00983B71A205BB4A1402B0502C56http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/19088195
http://purl.uniprot.org/uniprot/#_A0A0G2JWW3-mappedCitation-19088195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19088195
http://purl.uniprot.org/uniprot/#_A0A8L2QBV4-mappedCitation-19088195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19088195
http://purl.uniprot.org/uniprot/#_A0A2U8ZU93-mappedCitation-19088195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19088195
http://purl.uniprot.org/uniprot/#_B4DHJ7-mappedCitation-19088195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19088195
http://purl.uniprot.org/uniprot/#_F7FHM5-mappedCitation-19088195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19088195