Journal
JOURNAL OF CELL BIOLOGY
Volume 169, Issue 3, Pages 435-445Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200502019
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Funding
- NINDS NIH HHS [R01 NS014609, R56 NS014609, NS14609, R37 NS014609] Funding Source: Medline
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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- oragonist-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.
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