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Cytoplasmic calcium serves as a ubiquitous signal for acute cellular activation and for regulation of important cellular processes such as cell growth, division, differentiation, and even cell death and apoptosis. Increases in cytoplasmic calcium or calcium signals can be generated either by release of calcium from intracellular stores or by influx of calcium across the plasma membrane, but commonly by both means. The release of intracellular calcium comes from the endoplasmic reticulum or its specialized counterpart in muscle, the sarcoplasmic reticulum, and is generally signaled by the formation or influx of small mediators such as inositol 1,4,5-trisphosphate (IP3) (1), cyclic ADP ribose (2), and even calcium itself (3). Mechanisms for controlling calcium influx are somewhat more varied (4). Calcium influx can be more directly controlled by the membrane potential (5) or by the binding of extracellular neurotransmitters directly to the channels (6). Calcium influx can be signaled by second messengers such as cyclic nucleotides (7); however, in the case of receptors coupled to the phospholipase C pathway, the classical messengers of this pathway, IP3 and diacylglycerol, do not appear to be the primary mediators of activated calcium entry. Rather, in most instances, the signal for entry is somehow derived from the IP3-mediated depletion of calcium from intracellular stores, a process called “capacitative calcium entry” or “store-operated calcium entry” (8, 9). Two key issues regarding the mechanism of capacitative calcium entry have been (i) the nature of the signal from the endoplasmic reticulum that activates the channel, and (ii) the molecular identity of the channels themselves. It has been generally thought that the answer to the second question, the molecular identity of the channels, would likely lead to knowledge of the mechanism of signaling. Recent findings suggest that this may indeed be the case. In …

TRP, inositol 1,4,5-trisphosphate receptors, and capacitative calcium entry