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Store-operated calcium entry (SOCE) is a fundamental cellular mechanism that allows the influx of extracellular calcium ions into cells when the endoplasmic reticulum (ER) calcium stores are depleted. The two principal molecular components mediating SOCE are STIM1 (stromal interaction molecule 1) and Orai1, which together form the core of the highly selective calcium release-activated calcium (CRAC) channel system. STIM1 acts as a sensor for ER luminal calcium levels and upon store depletion, interacts with Orai1, a tetraspanin protein in the plasma membrane, triggering the opening of the CRAC channel and allowing calcium influx. This process is crucial for immune cell function, gene transcription, and neuronal excitability. Mutations or dysregulation of either component can lead to various pathologies due to impaired calcium signaling.
Modulation of store-operated calcium entry
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