Figure 1.

A scheme illustrating the standard mechanism and molecular components of SOCE in vascular smooth muscle cells. Store depletion by thapsigargin or vasoactive agonists binding to GPCR, induces Ca²⁺ store depletion, STIM1 organization in puncta and translocation to the plasma membrane, activation of Ca²⁺ entry through Orai1 and/or TRPC-dependent SOCC. A mechanism involving Orai1, TRPC1 and the voltage-sensitive Cav1.2, has also been implicated in Ca²⁺ influx induced by SOCE. Agonists also stimulate store independent Ca²⁺ entry through Orai1/3 activated by AA or LTC4; or through TRPC3/6/7 activated by DAG.