Annotated protein:Protein kinase C iota type (EC 2.7.11.13) (Atypical protein kinase C-lambda/iota) (aPKC-lambda/iota) (nPKC-iota). Gene symbol: PRKCI. Taxonomy: Rattus norvegicus (Rat). Uniprot ID: F1M7Y5
antibody wiki:
SynGO gene info:SynGO data @ PRKCI
Ontology domain:Biological Process
SynGO term:regulation of postsynaptic membrane neurotransmitter receptor levels (GO:0099072)
Synapse type(s):hippocampus, glutamatergic
Schaffer collateral synapse (CA3->CA1)
Annotated paper:Ren SQ, et al. "PKClambda is critical in AMPA receptor phosphorylation and synaptic incorporation during LTP" EMBO J. 2013 May 15;32(10):1365-80 PMID:23511975
Figure(s):Figure 1-3
Annotation description:This publication provides some evidence that PKC lambda/iota regulates the insertion of AMPAR at the PSD.
-A specific shRNA blocks the induction of LTP in hippocampal slices, which can be rescued by re-expression of PKC-lambda. (Figure 1)
-PI3K activation increases PKC lambda auto-phosphorylation and EPSC amplitudes. This is inhibited by PKC-lambda shRNA, and an inhibitor (Myr-aPKC-PS, more commonly known as ZIP) with some specificity to PKC-lambda. (Figure 2).
-PI3K activation leads to increased surface expression of GluRs, which is inhibited by Myr-aPKC-PS (Figure 3C-F).
-PI3K activation leads to increased mEPSC amplitudes, which can be blocked by PKC-lambda shRNA and Myr-aPKC-PS (Figure 3G-H).

It should be noted that at the concentration used, Myr-aPKC-PS also strongly inhibits PKC-zeta (see Figure 1D and Tsokas et al 2016). Thus, in several assays in this publication, it cannot be excluded that observed effects are mediated by PKC-zeta. The role of PKC-lambda in LTP is debated and likely involves an interplay with PKC-zeta expression (Tsokas et al 2016).
Evidence tracking, Biological System:Intact tissue
Cultured neurons
Evidence tracking, Protein Targeting:RNAi / shRNA
Antagonist / agonist
Evidence tracking, Experiment Assay:Confocal
Whole-cell patch clamp
Western blot
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:This publication provides additional discussion for the specificity of the inhibitors used. @ PMID:27187150
SynGO annotation ID:250
Dataset release (version):20231201
View annotation as GO-CAM model:Gene Ontology