Sonja Kampfer

TL;DR: A tentative model suggesting that, in the signaling pathway from Ha-Ras to the cytoskeleton aP KC-λ acts upstream of PI3K and Rac-1, whereas aPKC-ζ functions downstream of PI 3K and Race-1 is supported by studies demonstrating that cotransfection with plasmids encoding L61Ras and either aPK-λ or aPKR- ζ results in a stimulation of the kinase activity of both enzymes

TL;DR: Investigations revealed that cyclin D1 induction by transforming Ha-Ras is MEK- and Rac-dependent and requires the PKC isotypes ε, λ, and ζ, but not cPKC-α, while evidence is presented that aP KC-λ acts upstream of Rac, between Ras and Rac, whereas thePKC isotype ε andζ act downstream of Rac and are required for the activation of ERKs.

TL;DR: Co‐expression of oncogenic Ha‐Ras with combinations of kinase‐defective, dominant negative and constitutively active mutants of the various PKC isozymes are in agreement with a tentative model suggesting that, in the signaling pathway from Ha‐ Ras to the c‐fos promoter, aPKC‐λ acts upstream whereas aP KC‐ζ functions downstream of nPKC•ϵ.

TL;DR: Results confirm PKC θ to be the prime target for the activating effect of phorbol ester in T cell signaling and suggest that gene expression as well as gene function of PKCθ is strictly controlled by the cell type.

TL;DR: It is concluded that in NIH3T3 cells overexpressing the EGF receptor (EGFR6 cells), EGF requires cPKCα for the activation of the NHE, while calcium/calmodulin‐dependent kinases are essential in thapsigargin induced stimulation of theNHE.