Protein kinase C, zeta (PRKCZ) is a kinase required for insulin-dependent activation of AKT3, but may function as an adapter rather than a direct activator. Upon insulin treatment, it functions as a downstream effector of PI3K and contributes to the activation of translocation of the glucose transporter SLC2A4/GLUT4 and subsequent glucose transport in adipocytes. PRKCZ participates in TNF-dependent transactivation of NF-kappa-B by phosphorylating and activating IKBKB kinase, which in turn leads to the degradation of NF-kappa-B inhibitors. In migrating astrocytes, it forms a cytoplasmic complex with PARD6A and is recruited by CDC42 to function in the establishment of cell polarity along with the microtubule motor and dynein. In the inflammatory response, it is required for the T-helper 2 (Th2) differentiation process, including interleukin production, efficient activation of JAK1 and the subsequent phosphorylation and nuclear translocation of STAT6. Furthermore, in association with FEZ1, it stimulates neuronal differentiation in PC12 cells. In immunohistochemistry, it has membranous and cytoplasmic positivity throughout the body. References: The UniProt Consortium. Nucleic Acids Res. 47: D506-515 (2019); Nucleic Acids Res. 2016 Jan 4;44(D1):D733-45, PMID:26553804