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- W1879241542 endingPage "167" @default.
- W1879241542 startingPage "154" @default.
- W1879241542 abstract "From the very early days of nuclear factor-κB (NF-κB) research, it was recognized that different protein kinase C (PKC) isoforms might be involved in the activation of NF-κB. Pharmacological tools and pseudosubstrate inhibitors suggested that these kinases play a role in this important inflammatory and survival pathway; however, it was the analysis of several genetic mouse knockout models that revealed the complexity and interrelations between the different components of the PB1 network in several cellular functions, including T-cell biology, bone homeostasis, inflammation associated with the metabolic syndrome, and cancer. These studies unveiled, for example, the critical role of PKCζ as a positive regulator of NF-κB through the regulation of RelA but also its inflammatory suppressor activities through the regulation of the interleukin-4 signaling cascade. This observation is of relevance in T cells, where p62, PKCζ, PKCλ/ι, and NBR1 establish a mesh of interactions that culminate in the regulation of T-cell effector responses through the modulation of T-cell polarity. Many questions remain to be answered, not just from the point of view of the implication for NF-κB activation but also with regard to the in vivo interplay between these pathways in pathophysiological processes like obesity and cancer." @default.
- W1879241542 created "2016-06-24" @default.
- W1879241542 creator A5008277357 @default.
- W1879241542 creator A5037329333 @default.
- W1879241542 date "2012-03-01" @default.
- W1879241542 modified "2023-10-16" @default.
- W1879241542 title "The atypical PKCs in inflammation: NF-κB and beyond" @default.
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