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10.3389/fimmu.2015.00234

http://scihub22266oqcxt.onion/10.3389/fimmu.2015.00234
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C4440397!4440397!26052328
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suck abstract from ncbi


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pmid26052328      Front+Immunol 2015 ; 6 (ä): ä
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  • Tweeters, Woofers and Horns: The Complex Orchestration of Calcium Currents in T Lymphocytes #MMPMID26052328
  • Nohara LL; Stanwood SR; Omilusik KD; Jefferies WA
  • Front Immunol 2015[]; 6 (ä): ä PMID26052328show ga
  • Elevation of intracellular calcium ion (Ca2+) levels is a vital event that regulates T lymphocyte homeostasis, activation, proliferation, differentiation, and apoptosis. The mechanisms that regulate intracellular Ca2+ signaling in lymphocytes involve tightly controlled concinnity of multiple ion channels, membrane receptors, and signaling molecules. T cell receptor (TCR) engagement results in depletion of endoplasmic reticulum (ER) Ca2+ stores and subsequent sustained influx of extracellular Ca2+ through Ca2+ release-activated Ca2+ (CRAC) channels in the plasma membrane. This process termed store-operated Ca2+ entry (SOCE) involves the ER Ca2+ sensing molecule, STIM1, and a pore-forming plasma membrane protein, ORAI1. However, several other important Ca2+ channels that are instrumental in T cell function also exist. In this review, we discuss the role of additional Ca2+ channel families expressed on the plasma membrane of T cells that likely contribute to Ca2+ influx following TCR engagement, which include the TRP channels, the NMDA receptors, the P2X receptors, and the IP3 receptors, with a focus on the voltage-dependent Ca2+ (CaV) channels.
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