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Physiological function and molecular basis of STIM1‐mediated calcium entry in immune cells
Author(s) -
Baba Yoshihiro,
Kurosaki Tomohiro
Publication year - 2009
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/j.1600-065x.2009.00813.x
Subject(s) - stim1 , orai1 , microbiology and biotechnology , biology , endoplasmic reticulum , extracellular , intracellular , calcium signaling , cytosol , immune system , calcium , receptor , chemistry , immunology , biochemistry , enzyme , organic chemistry
Summary: Calcium signals in immune cells regulate a variety of physiological responses such as cell activation, differentiation, gene transcription, and effector functions. Surface receptor stimulation induces an increase in the concentration of cytosolic calcium ions (Ca 2+ ), which are derived mainly from two sources, intracellular endoplasmic reticulum (ER) Ca 2+ stores and the extracellular space. The major cascade for Ca 2+ entry in immune cells is through store‐operated Ca 2+ entry (SOCE) and Ca 2+ release‐activated Ca 2+ (CRAC) channels. Activation of SOCE is triggered by depletion of intracellular ER Ca 2+ stores, but the molecular mechanism was a long‐standing issue. With the recent molecular identification of the ER Ca 2+ sensor [stromal interacting molecule‐1 (STIM1)] and a pore‐forming subunit of the CRAC channel (Orai1), our understanding of the SOCE activation pathway has increased dramatically. These advances have now made it possible to shed some light on important questions: what is the physiological significance of SOCE, and what is its molecular basis? This review focuses on the recent progress in the field and the exciting opportunities for understanding how SOCE influences diverse immune functions.