Store-operated calcium signaling in neutrophils

被引：63

作者：

Clemens, Regina A. ^{[1
]}

Lowell, Clifford A. ^{[2
,3
]}

机构：

[1] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA

[3] Univ Calif San Francisco, Program Immunol, San Francisco, CA 94143 USA

来源：

JOURNAL OF LEUKOCYTE BIOLOGY | 2015年 / 98卷 / 04期

基金：

美国国家卫生研究院;

关键词：

sensors; channels; NADPH oxidase; neutrophil activation; INTRACELLULAR CA2+ STORES; CHANNEL FUNCTION; SENSORS STIM1; PORE SUBUNIT; MICE LACKING; CRAC CHANNEL; HL-60; CELLS; MAST-CELLS; T-CELL; ACTIVATION;

D O I：

10.1189/jlb.2MR1114-573R

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Calcium signals in neutrophils are initiated by a variety of cell-surface receptors, including formyl peptide and other GPCRs, FcRs, and integrins. The predominant pathway by which calcium enters immune cells is termed SOCE, whereby plasmamembrane CRAC channels allow influx of extracellular calcium into the cytoplasm when intracellular ER stores are depleted. The identification of 2 key families of SOCE regulators, STIM calcium "sensors" and ORAI calcium channels, has allowed for genetic manipulation of SOCE pathways and provided valuable insight into the molecularmechanism of calcium signaling in immune cells, including neutrophils. This review focuses on our current knowledge of the molecules involved in neutrophil SOCE and how study of these molecules has further informed our understanding of the role of calcium signaling in neutrophil activation.

引用

页码：497 / 502

页数：6

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