CRAC channels in secretory epithelial cell function and disease. (March 2019)

• Record Type: Journal Article
• Authors: Liu, Haiping; Kabrah, Ahmed; Ahuja, Malini; Muallem, Shmuel
• Is Part Of: Cell calcium. Volume 78(2019)
• Page Start: 48
• Page End: 55
• Publication Date: 2019-03
• Subjects: Secretory cells -- Orai1 -- TRPC channels -- Ca2+ influx -- Toxicity; Calcium -- Metabolism -- Periodicals; Vertebrates -- Physiology -- Periodicals; Calcium -- Physiological effect -- Periodicals; Cell physiology -- Periodicals; Calcium in the body -- Periodicals; 572.516
• DOI: 10.1016/j.ceca.2018.12.010
• Languages: English
• ISSNs: 0143-4160

Abstract

Graphical abstract: Highlights: -Ca 2+ signaling in secretory epithelia. -Ca 2+ influx and cell functions in secretory epithelia. -Ca 2+ influx and disease in secretory epithelia. Abstract: The receptor-evoked Ca 2+ signal in secretory epithelia mediate many cellular functions essential for cell survival and their most fundamental functions of secretory granules exocytosis and fluid and electrolyte secretion. Ca 2+ influx is a key component of the receptor-evoked Ca 2+ signal in secretory cell and is mediated by both TRPC and the STIM1-activated Orai1 channels that mediates the Ca 2+ release-activated current (CRAC) Icrac . The core components of the receptor-evoked Ca 2+ signal are assembled at the ER/PM junctions where exchange of materials between the plasma membrane and internal organelles take place, including transfer of lipids and Ca 2+ . The Ca 2+ signal generated at the confined space of the ER/PM junctions is necessary for activation of the Ca 2+ -regulated proteins and ion channels that mediate exocytosis with high fidelity and tight control. In this review we discuss the general properties of Ca 2+ signaling, PI(4, 5)P2 and other lipids at the ER/PM junctions with regard to secretory cells function and disease caused by uncontrolled Ca 2+ influx.