Matches in Nanopublications for { ?s ?p "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." ?g. }
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- _5 value "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." provenance.
- _5 value "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." provenance.