PRKCZ, is a protein that in humans is encoded by the PRKCZ gene. The PRKCZ gene encodes at least two alternative transcripts, the full-length PKCζ and an N-terminal truncated form PKMζ. PKMζ is thought to be responsible for maintaining long-term memories in pkc iota brain.
PKC-zeta has an N-terminal regulatory domain, followed by a hinge region and a C-terminal catalytic domain. PKMζ is the independent catalytic domain of PKCζ and, lacking an autoinhibitory regulatory domain of the full-length PKCζ, is constitutively and persistently active, without the need of a second messenger. Inhibition of the PKCζ enzyme inhibits insulin-stimulated glucose transport while activation of PKCζ increases glucose transport. Alteration in PKMζ may be involved in neurodegeneration Alzheimer’s disease. Model organisms have been used in the study of PRKCZ function.
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Persistent activation of the zeta isoform of protein kinase C in the maintenance of long-term potentiation”. Proceedings of the National Academy of Sciences of the United States of America. Protein kinase M zeta synthesis from a brain mRNA encoding an independent protein kinase C zeta catalytic domain. Implications for the molecular mechanism of memory”.
PKC-zeta mediates insulin effects on glucose transport in cultured preadipocyte-derived human adipocytes”. Protein kinase Mzeta is necessary and sufficient for LTP maintenance”. Persistent phosphorylation by protein kinase Mzeta maintains late-phase long-term potentiation”. Storage of spatial information by the maintenance mechanism of LTP”. Plasticity in the human central nervous system”.