Physiological function and molecular basis of STIM1-mediated calcium entry in immune cells

被引:42
作者
Baba, Yoshihiro [1 ,2 ]
Kurosaki, Tomohiro [1 ,2 ]
机构
[1] Osaka Univ, WPI Immunol Frontier Res Ctr, Lab Lymphocyte Differentiat, Suita, Osaka 5650871, Japan
[2] RIKEN, Res Ctr Allergy & Immunol, Lab Lymphocyte Differentiat, Kanagawa, Japan
关键词
store-operated calcium entry; STIM1; Orai1; mast cells; immune cells; OPERATED CA2+ ENTRY; RECEPTOR-MEDIATED PHAGOCYTOSIS; ACTIVATED PROTEIN-KINASE; STORE-INDEPENDENT MODES; CRAC CHANNEL ACTIVATION; JUN NH2-TERMINAL KINASE; SIGNAL-REGULATED KINASE; PLASMA-MEMBRANE; MAST-CELLS; T-CELL;
D O I
10.1111/j.1600-065X.2009.00813.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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<SU2+</SU), which are derived mainly from two sources, intracellular endoplasmic reticulum (ER) Ca<SU2+</SU stores and the extracellular space. The major cascade for Ca<SU2+</SU entry in immune cells is through store-operated Ca<SU2+</SU entry (SOCE) and Ca<SU2+</SU release-activated Ca<SU2+</SU (CRAC) channels. Activation of SOCE is triggered by depletion of intracellular ER Ca<SU2+</SU stores, but the molecular mechanism was a long-standing issue. With the recent molecular identification of the ER Ca<SU2+</SU 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.
引用
收藏
页码:174 / 188
页数:15
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