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XB-ART-5101
J Biol Chem 2003 Sep 05;27836:33730-7. doi: 10.1074/jbc.M305023200.
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Ca2+-calmodulin-dependent protein kinase II potentiates store-operated Ca2+ current.

Machaca K .


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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.

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Species referenced: Xenopus laevis
Genes referenced: camk2g

References [+] :
Barrett, Stimulation of unitary T-type Ca(2+) channel currents by calmodulin-dependent protein kinase II. 2000, Pubmed