Ca super(2+)-Calmodulin-dependent Protein Kinase II Potentiates Store- operated Ca super(2+) Current

A rise in intracellular Ca super(2+) (Ca super(2+) sub(i)) mediates various cellular functions ranging from fertilization to gene expression. A ubiquitous Ca super(2+) influx pathway that contributes significantly to the generation of Ca super(2+) sub(i) signals, especially in non-excitable cells, i...

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Bibliographic Details
Published in:The Journal of biological chemistry 2003-09, Vol.278 (36), p.33730-33737
Main Author: Machaca, K
Format: Article
Language:English
Online Access:Get full text
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Summary:A rise in intracellular Ca super(2+) (Ca super(2+) sub(i)) mediates various cellular functions ranging from fertilization to gene expression. A ubiquitous Ca super(2+) influx pathway that contributes significantly to the generation of Ca super(2+) sub(i) signals, especially in non-excitable cells, is store-operated Ca super(2+) entry (SOCE). Consequently, the modulation of SOCE current affects Ca super(2+) sub(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 Ca super(2+) sub(i) potentiates SOCE. This potentiation is mediated by Ca super(2+)-calmodulin-dependent protein kinase II (CaMKII), because inhibition of endogenous CaMKII activity abrogates Ca super(2+) sub(i)-mediated SOCE potentiation and expression of constitutively active CaMKII potentiates SOCE current independently of Ca super(2+) sub(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.
ISSN:0021-9258
DOI:10.1074/jbc.M305023200