STIM1, an Essential and Conserved Component of Store-Operated Ca2+ Channel FunctionJournal of Cell Biology
AbstractStore-operated Ca2+ (SOC) channels regulate many cellular processes, but the underlying molecular components are not well defined. Using an RNA interference (RNAi)-based screen to identify genes that alter thapsigargin (TG)-dependent Ca2+ entry, we discovered a required and conserved role of Stim in SOC influx. RNAi-mediated knockdown of Stim in Drosophila S2 cells significantly reduced TG-dependent Ca2+ entry. Patch-clamp recording revealed nearly complete suppression of the Drosophila Ca2+ release-activated Ca2+(CRAC) current that has biophysical characteristics similar to CRAC current in human T cells. Similarly, knockdown of the human homologue STIM1 significantly reduced CRAC channel activity in Jurkat T cells. RNAi-mediated knockdown of STIM1 inhibited TG- or agonist-dependent Ca2+ entry in HEK293 or SH-SY5Y cells. Conversely, overexpression of STIM1 in HEK293 cells modestly enhanced TG-induced Ca2+ entry. We propose that STIM1, a ubiquitously expressed protein that is conserved from Drosophila to mammalian cells, plays an essential role in SOC influx and may be a common component of SOC and CRAC channels.
Citation InformationJack Roos, Paul J. DiGregorio, Andriy V. Yeromin, Kari Ohlsen, et al.. "STIM1, an Essential and Conserved Component of Store-Operated Ca2+ Channel Function" Journal of Cell Biology Vol. 169 Iss. 3 (2005) p. 435 - 445 ISSN: 0021-9525
Available at: http://works.bepress.com/j_kozak/34/