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|Title:||Atypical Protein Kinase C (PKCλ/ζ) is a convergent downstream target of the insulin stimulated phosphatidylinositol 3-kinase and TC10 signalling pathways|
Mora Fayos, Sílvia
Hwang, Joseph B.
Saltiel, Alan R.
Pessin, Jeffrey E.
|Publisher:||Rockefeller University Press|
|Abstract:||Insulin stimulation of adipocytes resulted in the recruitment of atypical PKC (PKCζ/λ) to plasma membrane lipid raft microdomains. This redistribution of PKCζ/λ was prevented by Clostridium difficile toxin B and by cholesterol depletion, but was unaffected by inhibition of phosphatidylinositol (PI) 3-kinase activity. Expression of the constitutively active GTP-bound form of TC10 (TC10Q/75L), but not the inactive GDP-bound mutant (TC10/T31N), targeted PKCζ/λ to the plasma membrane through an indirect association with the Par6-Par3 protein complex. In parallel, insulin stimulation as well as TC10/Q75L resulted in the activation loop phosphorylation of PKCζ. Although PI 3-kinase activation also resulted in PKCζ/λ phosphorylation, it was not recruited to the plasma membrane. Furthermore, insulin-induced GSK-3β phosphorylation was mediated by both PI 3-kinase-PKB and the TC10-Par6-atypical PKC signaling pathways. Together, these data demonstrate that PKCζ/λ can serve as a convergent downstream target for both the PI 3-kinase and TC10 signaling pathways, but only the TC10 pathway induces a spatially restricted targeting to the plasma membrane.|
|Note:||Reproducció del document publicat a: https://doi.org/10.1083/jcb.200306152|
|It is part of:||Journal of Cell Biology, 2004, vol. 164, p. 279-290|
|Appears in Collections:||Articles publicats en revistes (Bioquímica i Biomedicina Molecular)|
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