Role of Drosophila TRP in inositide-mediated Ca2+ entry.
Inositol lipid signaling relies on an InsP3-induced Ca2+ release from intracellular stores and on extracellular Ca2+ entry, which takes place when the Ca2+ stores become depleted of Ca2+. This interplay between Ca2+ release and Ca2+ entry has been termed capacitative Ca2+ entry and the inward current calcium release activated current (CRAC) to indicate gating of Ca2+ entry by Ca2+-store depletion. The signaling pathway and the gating mechanism of capacitative Ca2+ entry, however, are largely unknown and the molecular participants in this process have not been identified. In this article we review genetic, molecular, and functional studies of wild-type and mutant Drosophila photoreceptors, suggesting that the transient receptor potential mutant ( trp) is the first putative capacitative Ca2+ entry mutant. Furthermore, several lines of evidence suggest that the trp gene product TRP is a candidate subunit of the plasma membrane channel that is activated by Ca2+ store depletion.[1]References
- Role of Drosophila TRP in inositide-mediated Ca2+ entry. Minke, B., Selinger, Z. Mol. Neurobiol. (1996) [Pubmed]
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