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   <subfield code="a">Role of Drosophila TRP in inositide-mediated Ca2+ entry</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Baruch Minke, Zvi Selinger]</subfield>
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   <subfield code="a">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 mutantDrosophila photoreceptors, suggesting that thetransient receptor potential mutant (trp) is the first putative capacitative Ca2+ entry mutant. Furthermore, several lines of evidence suggest that thetrp gene product TRP is a candidate subunit of the plasma membrane channel that is activated by Ca2+ store depletion.</subfield>
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   <subfield code="a">Ca2+ mobilization</subfield>
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