Juan A Rosado
Posters-Accepted Abstracts: Biol Syst Open Access
Introduction: Agonist-induced depletion of the intracellular Ca2+ stores leads to the initiation of a signaling cascade that results in the opening of plasma membrane Ca2+-permeable channels. The so-called store-operated Ca2+ entry (SOCE) is a major mechanism for Ca2+ influx regulated by the filling state of the agonist-sensitive Ca2+ pools. Ca2+ influx via SOCE is required for the maintenance of sustained elevations in cytosolic Ca2+ concentrations, required for the full activation of a number of physiological events, and to refill the intracellular stores. The mechanism underlying the communication of the filling state of the Ca2+ stores to the plasma membrane channels, as well as the nature of the channels have been a matter of intense research in the last three decades. STIM1, an EF-hand containing protein located in the membrane of the endoplasmic reticulum and other agonist-sensitive stores, as well as the plasma membrane, has been reported to communicate the information of the filling state of the Ca2+ stores to the store-operated channels. STIM1 has been found to activate two types of store-operated channels, Orai1, which has been reported to mediate the Ca2+ release-activated Ca2+-selective current, ICRAC, and TRPC channels, which conduct the non-voltage activated, non Ca2+-selective ISOC current. Despite both Orai and TRPC channels have been found to be activated by STIM1 upon depletion of the intracellular Ca2+ stores and contribute to conduct SOCE in different cell types, current evidence support that both types of channels have specific and non-overlapping physiological functions.
