Abstract
Store-operated Ca2+ entry (SOCE) due to activation of Ca2+-release-activated Ca2+ (CRAC) channels leads to sustained elevation of cytoplasmic Ca2+ and activation of lymphocytes. CRAC channels consisting of four pore-forming Orai1 subunits are activated by STIM1, an endoplasmic reticulum Ca2+ sensor that senses intracellular store-depletion and migrates to plasma membrane proximal regions to mediate SOCE. One of the fundamental properties of CRAC channels is their Ca2+-dependent fast inactivation (CDI).
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