Lifting the fog in store-operated Ca2+ entry

Immunoreceptor signalling leads to Ca2+ release from intracellular stores, which is followed by the entry of external Ca2+ into the cell through mysterious store-operated Ca2+ (SOC) channels. Recent studies have identified stromal interaction molecules (STIMs) as having an essential role in SOC influx. Remarkably, Ca2+ store depletion induces a rapid redistribution of the endoplasmic reticulum STIM1 into puncta that accumulate near the plasma membrane. The combined data suggest that STIM1 functions as a Ca2+ sensorin the signalling pathways connecting Ca2+ store depletion to SOC entry.