PUBLICATION

Phosphorylation and activation of nuclear Ca(2+)/calmodulin-dependent protein kinase phosphatase (CaMKP-N/PPM1E) by Ca(2+)/calmodulin-dependent protein kinase I (CaMKI)

Authors
Onouchi, T., Sueyoshi, N., Ishida, A., and Kameshita, I.
ID
ZDB-PUB-120529-42
Date
2012
Source
Biochemical and Biophysical Research Communications   422(4): 703-709 (Journal)
Registered Authors
Keywords
CaM kinase, CaMKP-N/PPM1E, CaMKP/PPM1F, protein phosphorylation, proteolytic processing, translocation
MeSH Terms
  • Alanine/genetics
  • Alanine/metabolism
  • Amino Acid Sequence
  • Amino Acid Substitution
  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 1/metabolism*
  • Cell Line, Tumor
  • Enzyme Activation
  • Mice
  • Molecular Sequence Data
  • Mutation
  • Phosphoprotein Phosphatases/genetics
  • Phosphoprotein Phosphatases/metabolism*
  • Phosphorylation
  • Rats
  • Recombinant Proteins/genetics
  • Recombinant Proteins/metabolism
  • Serine/genetics
  • Serine/metabolism
PubMed
22627141 Full text @ Biochem. Biophys. Res. Commun.
Abstract

Nuclear Ca2+/calmodulin-dependent protein kinase phosphatase (CaMKP-N/PPM1E) is an enzyme that dephosphorylates and downregulates multifunctional Ca2+/calmodulin-dependent protein kinases (CaMKs) as well as AMP-dependent protein kinase. In our previous study, we found that zebrafish CaMKP-N (zCaMKP-N) underwent proteolytic processing and translocated to cytosol in a proteasome inhibitor-sensitive manner. In the present study, we found that zCaMKP-N is regulated by phosphorylation at Ser-480. When zCaMKP-N was incubated with the activated CaMKI, time-dependent phosphorylation of the enzyme was observed. This phosphorylation was significantly reduced when Ser-480 was replaced by Ala, suggesting that CaMKI phosphorylates Ser-480 of zCaMKP-N. Phosphorylation-mimic mutants, S480D and S480E, showed higher phosphatase activities than those of wild type and S480A mutant in solution-based phosphatase assay using various substrates. Furthermore, autophosphorylation of CaMKII after ionomycin treatment was more severely attenuated in Neuro2a cells when CaMKII was cotransfected with the phosphorylation-mimic mutant of zCaMKP-N than with the wild-type or non-phosphorylatable zCaMKP-N. These results strongly suggest that phosphorylation of zCaMKP-N at Ser-480 by CaMKI activates CaMKP-N catalytic activity and thereby downregulates multifunctional CaMKs in the cytosol.

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