Ca2+-Calmodulin-dependent Protein Kinase II Potentiates Store-operated Ca2+ Current

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

A rise in intracellular Ca2+ (Ca2+i) mediates various cellular functions ranging from fertilization to gene expression. A ubiquitous Ca2+ influx pathway that contributes significantly to the generation of Ca2+i signals, especially in non-excitable cells, is store-operated Ca2+ entry (SOCE). Consequently, the modulation of SOCE current affects Ca 2+i dynamics and thus the ensuing cellular response. Therefore, it is important to define the mechanisms that regulate SOCE. Here we show that a rise in Ca2+i potentiates SOCE. This potentiation is mediated by Ca2+-calmodulin-dependent protein kinase II (CaMKII), because inhibition of endogenous CaMKII activity abrogates Ca 2+i-mediated SOCE potentiation and expression of constitutively active CaMKII potentiates SOCE current independently of Ca 2+i. Moreover, we present evidence that CaMKII potentiates SOCE by altering SOCE channel gating. The regulation of SOCE by CaMKII defines a novel modulatory mechanism of SOCE with important physiological consequences.

Original languageEnglish
Pages (from-to)33730-33737
Number of pages8
JournalJournal of Biological Chemistry
Volume278
Issue number36
DOIs
Publication statusPublished - 5 Sep 2003

    Fingerprint

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this