Kanzaki, MakotoMora Fayos, SílviaHwang, Joseph B.Saltiel, Alan R.Pessin, Jeffrey E.2021-04-262021-04-262004-01-200021-9525https://hdl.handle.net/2445/176748Insulin 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.12 p.application/pdfengcc-by (c) Kanzaki, Makoto et al., 2004http://creativecommons.org/licenses/by/3.0/esInsulinaFosforilacióInsulinPhosphorylationinfo:eu-repo/semantics/article7115222021-04-26info:eu-repo/semantics/openAccess14734537