|Citation||Roos, J., DiGregorio, P.J., Yeromin, A.V., Ohlsen, K., Lioudyno, M., Zhang, S., Safrina, O., Kozak, J.A., Wagner, S.L., Cahalan, M.D., Velicelebi, G., Stauderman, K.A. (2005). STIM1, an essential and conserved component of store-operated Ca2+ channel function. J. Cell Biol. 169(3): 435--445. (Export to RIS)|
|Publication Type||Research paper|
|PubMed Abstract||Store-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.|
|Review||Capacitative calcium entry: sensing the calcium stores.
Putney, 2005, J. Cell Biol. 169(3): 381--382 [FBrf0187822]
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|Language of Publication||English|
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|Also Published As|
|Abbreviation||J. Cell Biol.|
|Title||Journal of Cell Biology|
|Data from Reference|