Abstract: The activation of Ca²⁺ entry through store-operated channels by agonists that deplete Ca²⁺ from the endoplasmic reticulum (ER) is a ubiquitous signaling mechanism, the molecular basis of which has remained elusive for the past two decades. Store-operated Ca²⁺-release-activated Ca²⁺ (CRAC) channels constitute the sole pathway for Ca²⁺ entry following antigen-receptor engagement. In a set of breakthrough studies over the past two years, stromal interaction molecule 1 (STIM1, the ER Ca²⁺ sensor) and Orai1 (a pore-forming subunit of the CRAC channel) have been identified. Here we review these recent studies and the insights they provide into the mechanism of store-operated Ca²⁺ channels (SOCCs).

Key words: Store-operated Ca²⁺ entry (SOCE), Stromal interaction molecule (STIM), Orai

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