| Annotated protein: | Protein kinase C zeta type (EC 2.7.11.13) (nPKC-zeta). Gene symbol: PRKCZ. Taxonomy: Rattus norvegicus (Rat). Uniprot ID: P09217 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ PRKCZ |
| Ontology domain: | Biological Process |
| SynGO term: | regulation of neurotransmitter receptor localization to postsynaptic specialization membrane (GO:0098696) |
| Synapse type(s): | hippocampus, glutamatergic Schaffer collateral synapse (CA3->CA1) |
| Annotated paper: | Yao Y, et al. "PKM zeta maintains late long-term potentiation by N-ethylmaleimide-sensitive factor/GluR2-dependent trafficking of postsynaptic AMPA receptors" J Neurosci. 2008 Jul 30;28(31):7820-7 PMID:18667614 |
| Figure(s): | Figure 1,3 |
| Annotation description: | It is shown that postsynaptic perfusion with PKM zeta (a constitutively active splice variant of the PRKCZ gene) increases postsynaptic AMPAR responses. This is inhibited by pep2m, a peptide that inhibits NSF/GluR2 interactions (Figure 1). The effect does not require exocytotic insertion of GluRs, since Botox B is unable to inhibit the effect (Figure 1D), and there is no increase in the surface or total level or GluR2 (Figure 3E). Using synaptosomes, it is shown that PKM-zeta dependent LTP does lead to a increase in synaptic GluR2 and GluR3, and that this is blocked by pep2m and a ZIP (a inhibitor with some specificity to PKM-zeta). It is thus concluded that PKM-zeta increases AMPAR responses by recruiting extrasynaptic GluRs to the PSD. Ling et.al. 2006 demonstrates that PKM zeta-induced potentiation requires an increase in the number of receptors, not an increase in receptor conductance. It should be noted that PKM-zeta has long been suspected to be essential for postsynaptic LTP, but that this is subject on an ongoing debate. (Tsokas et.al. 2016). |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Over-expression |
| Evidence tracking, Experiment Assay: | Whole-cell patch clamp Field recordings |
| Annotator(s): | Arthur de Jong (ORCID:0000-0002-7620-2704) Pascal Kaeser (ORCID:0000-0002-1558-1958) |
| Lab: | Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA |
| Additional literature: | It is shown that PKM-zeta mediated potentiation of AMPAR currents is dependent on the recruitment of additional receptors, and not by increased receptor conductance. @ PMID:16463388 This publication shows a role for PKM-zeta in postsynaptic LTP, and discusses compensatory mechanisms in PKM-zeta knockouts. @ PMID:27187150 Volk et.al. demonstrated that PKM-zeta knockout alone is not sufficient to abolish LTP. This is an important reference together with Tsokas 2016. @ PMID:23283174 |
| SynGO annotation ID: | 249 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |