摘要
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).
The activation of Ca^2＋ entry through store-operated channels by agonists that deplete Ca^2＋ 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 Ca^2＋-release-activated Ca^2＋ （CRAC） channels constitute the sole pathway for Ca^2＋ entry following antigen-receptor engagement. In a set of breakthrough studies over the past two years, stromal interaction molecule 1 （STIM 1, the ER Ca^2＋ sensor） and Orai 1 （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 Ca^2＋ channels （SOCCs）.
