Capacitative calcium entry: from concept to molecules

Abstract

Summary: Rapid to moderately rapid changes in intracellular Ca 2+concentration, or Ca 2+signals, control a variety of critical cellular functions in the immune system. These signals are comprised of Ca 2+release from intracellular stores coordinated with Ca 2+influx across the plasma membrane. The most common mechanisms by which these two modes of signaling occur is through inositol 1,4,5‐trisphosphate (IP 3)‐induced release of Ca 2+from the endoplasmic reticulum (ER) and store‐operated Ca 2+entry across the plasma membrane. The latter process was postulated over 20 years ago, and in just the past few years, the key molecular players have been discovered: STIM proteins serve as sensors of Ca 2+within the ER which communicate with and activate plasma membrane store‐operated channels composed of Orai subunits. The process of store‐operated Ca 2+entry provides support for oscillating Ca 2+signals from the ER and also provides direct activator Ca 2+that signals to a variety of downstream effectors.