Laura Sanz

TL;DR: It is demonstrated that the inhibition of the aPKCs or the down‐regulation of p62 severely abrogates NF‐κB activation by IL‐1 and TRAF6, suggesting that both proteins are critical intermediaries in this pathway.

TL;DR: It is demonstrated that the interaction of p62 with RIP serves to link the atypical PKCs to the activation of NF‐κB by the TNFα signaling pathway.

TL;DR: The role that zetaPKC plays in NF-kappaB activation is addressed using mice in which this kinase was inactivated by homologous recombination and these mice, although grossly normal, showed phenotypic alterations in secondary lymphoid organs reminiscent of those of the TNF receptor-1 and of the lymphotoxin-beta receptor gene-deficient mice.

TL;DR: Results are shown here demonstrating that the expression of par-4 in NIH-3T3 cells induces morphological changes typical of apoptosis, which are abrogated by cotransfection of either wild-type zeta PKC or lambda/LPKC, but not by their respective kinase-inactive mutants.

TL;DR: Experimental evidence is presented demonstrating that activation of zeta PKC is not only necessary but also sufficient by itself to activate maturation in oocytes and to produce deregulation of growth control in mouse fibroblasts, and proposing zETA PKC as a critical step downstream of p21ras in mitogenic signal transduction.