Ca2+-calmodulin-dependent protein kinase II potentiates store-operated Ca2+ current. Academic Article uri icon

Overview

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 Ca2+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 Ca2+i-mediated SOCE potentiation and expression of constitutively active CaMKII potentiates SOCE current independently of Ca2+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.

publication date

  • June 22, 2003

Research

keywords

  • Calcium
  • Calcium Channels
  • Calcium-Calmodulin-Dependent Protein Kinases

Identity

PubMed Central ID

  • PMC1282465

Scopus Document Identifier

  • 0141817997

PubMed ID

  • 12821654

Additional Document Info

volume

  • 278

issue

  • 36