期刊
SCIENCE
卷 312, 期 5777, 页码 1220-1223出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1127883
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资金
- NIAID NIH HHS [R01-AI050200, R01 AI050200] Funding Source: Medline
- NIGMS NIH HHS [R01-GM065360, R01 GM065360, 5-R37-GM053950, R37 GM053950] Funding Source: Medline
- NINDS NIH HHS [R01 NS040927, R01-NS040927] Funding Source: Medline
Store-operited Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (CRAC) channels following Ca2+ release from intracellular stores. We performed a genome-wide RNA interference (RNAi) screen in Drosophila cells to identify proteins that inhibit store-operated Ca2+ influx. A secondary patch-clamp screen identified CRACM1 and CRACM2 (CRAC modulators 1 and 2) as modulators of Drosophila CRAC currents. We characterized the human ortholog of CRACM1, a plasma membrane-resident protein encoded by gene FLJ14466. Although overexpression of CRACM1 did not affect CRAC currents, RNAi-mediated knockdown disrupted its activation. CRACM1 could be the CRAC channel itself, a subunit of it, or a component of the CRAC signaling machinery.
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