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Mechanisms of capacitative calcium entry

Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, NIH, Research Triangle, Park, NC 27709, USA

*Author for correspondence (e-mail: putney{at}niehs.nih.gov)

Capacitative Ca²⁺ entry involves the regulation of plasma membrane Ca²⁺ channels by the filling state of intracellular Ca²⁺ stores in the endoplasmic reticulum (ER). Several theories have been advanced regarding the mechanism by which the stores communicate with the plasma membrane. One such mechanism, supported by recent findings, is conformational coupling: inositol 1,4,5-trisphosphate (Ins(1,4,5)P₃) receptors in the ER may sense the fall in Ca²⁺ levels through Ca²⁺-binding sites on their lumenal domains, and convey this conformational information directly by physically interacting with Ca²⁺ channels in the plasma membrane. In support of this idea, in some cell types, store-operated channels in excised membrane patches appear to depend on the presence of both Ins(1,4,5)P₃ and Ins(1,4,5)P₃ receptors for activity; in addition, inhibitors of Ins(1,4,5)P₃ production that either block phospholipase C or inhibit phosphatidylinositol 4-kinase can block capacitative Ca²⁺ entry. However, the electrophysiological current underlying capacitative Ca²⁺ entry is not blocked by an Ins(1,4,5)P₃ receptor antagonist, and the blocking effects of a phospholipase C inhibitor are not reversed by the intracellular application of Ins(1,4,5)P₃. Furthermore, cells whose Ins(1,4,5)P₃ receptor genes have been disrupted can nevertheless maintain their capability to activate capacitative Ca²⁺ entry channels in response to store depletion. A tentative conclusion is that multiple mechanisms for signaling capacitative Ca²⁺ entry may exist, and involve conformational coupling in some cell types and perhaps a diffusible signal in others.

Key words: Calcium channels, Capacitative calcium entry, Calcium signaling, Signal transduction

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