Reference Report
| Reference | |||
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| 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) | ||
| FlyBase ID | FBrf0187823 | ||
| Publication Type | Research paper | ||
| PubMed ID | 15866891 | ||
| 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. | ||
| DOI | |||
| Related Publication(s) | |||
| 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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| Publication Type | Journal | ||
| Abbreviation | J. Cell Biol. | ||
| Title | Journal of Cell Biology | ||
| Publication Year | 1966- | ||
| ISBN/ISSN | 0021-9525 | ||
Data from Reference
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Genes (21)
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