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Stimulation of cells with physiological concentrations of calcium-mobilizing agonists often results in the generation of repetitive cytoplasmic Ca(2+) oscillations. Although oscillations arise from regenerative Ca(2+) release, they are sustained by store-operated Ca(2+) entry through Ca(2+) release-activated Ca(2+) (CRAC) channels. Here, we show that following stimulation of cysteinyl leukotriene type I receptors in rat basophilic leukemia (RBL)-1 cells, large amplitude Ca(2+) oscillations, CRAC channel activity, and downstream Ca(2+)-dependent nuclear factor of activated T cells (NFAT)-driven gene expression are all exclusively maintained by the endoplasmic reticulum Ca(2+) sensor stromal interaction molecule (STIM) 1. However, stimulation of tyrosine kinase-coupled FCεRI receptors evoked Ca(2+) oscillations and NFAT-dependent gene expression through recruitment of both STIM2 and STIM1. We conclude that different agonists activate different STIM proteins to sustain Ca(2+) signals and downstream responses.

Original publication

DOI

10.1073/pnas.1201204109

Type

Journal article

Journal

Proc Natl Acad Sci U S A

Publication Date

01/05/2012

Volume

109

Pages

6969 - 6974

Keywords

Animals, Calcium Channels, Calcium Signaling, Calcium-Binding Proteins, Cell Line, Tumor, Gene Expression, Gene Knockdown Techniques, Leukotriene C4, Membrane Glycoproteins, Membrane Proteins, NFATC Transcription Factors, Rats, Receptors, Leukotriene