Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Academic Editor: Hector Valdivia
The store-operated Ca2+ channel (SOC) located on the plasma membrane (PM) mediates capacitative entry of extracellular Ca2+ following depletion of intracellular Ca2+ stores in the endoplasmic or sarcoplasmic reticulum (ER/SR). It plays important roles in a variety of cell signaling processes, including proliferation, apoptosis, gene regulation and motility. In skeletal muscle, the L-type Ca2+ channel on the surface membrane has slow kinetics of activation in response to voltage stimulation, and therefore does not support entry of extracellular Ca2+. Recent studies have provided functional evidence for the existence of SOC in muscle cells. Severe dysfunction of SOC is identified in muscle cells lacking either ryanodine receptors located on the SR membrane, or mitsugumin 29 - a membrane protein located in the triad junction of skeletal muscle. These results indicate that SOC activation requires an intact interaction between PM and SR, and is linked to conformational changes of ryanodine receptors. The cumulative entry of Ca2+ through SOC not only provides the mechanism for refilling of intracellular Ca2+ stores, but may also add to the Ca2+ needed for muscle contraction under conditions of intensive exercise and fatigue. The proper coupling of PM with ER/SR, in the triad junction in skeletal muscle or dyad junction in cardiac muscle, is essential not only for the membrane excitation-induced intracellular Ca2+ release but also for the store depletion-initiated capacitative Ca2+ entry.