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http://amigo.geneontology.org/amigo/term/GO:0016301
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p(HGNC:TNF) -> kin(p(HGNC:PRKCZ))
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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1.4
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Jung et al. [36] recently investigated TNF-a-induced HIF-1a accumulation and demonstrated that an NFkB-mediated event that is normally associated with inflammation and cell survival caused protein accumulation in normoxic cells. Although the report fails to identify the mechanism of HIF-1a accumulation, it is suggested that this might interfere with the pVHL-mediated HIF-1a degradation process. Further studies support the concept of a pVHL-dependent cytotoxicity to TNF-a in RCC cells [37,38]. In particular, it has been reported that RCC cells can be sensitized to TNF-a-induced cytotoxicity by re-introducing wild-type VHL [38]. The authors highlight the fact that TNFreceptor engagement by TNF-a triggers the activation of atypical protein kinase C (aPKC), which, through IKKb phosphorylation, liberates NFkB, thereby initiating the transcription of genes that are involved in apoptosis.
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Selventa
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2014-07-03T14:30:27.339+02:00
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