Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 14, Issue 10, Pages 2337-2349Publisher
WILEY
DOI: 10.1111/j.1582-4934.2010.01168.x
Keywords
store-operated Ca2+entry; CRAC; calcium influx; calcium channel; STIM1; STIM2; Orai1; Orai2; Orai3; TRPC
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Funding
- NIH, National Institute of Environmental Health Sciences
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [ZIAES090087] Funding Source: NIH RePORTER
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Introduction I-CRAC Orais STIM1 STIM2 STIM1, STIM2 and Ca2+ oscillations TRPCs and SOCE Conclusions The process of store-operated Ca2+ entry (SOCE), whereby Ca2+ influx across the plasma membrane is activated in response to depletion of intracellular Ca2+ stores in the endoplasmic reticulum (ER), has been under investigation for greater than 25 years; however, only in the past 5 years have we come to understand this mechanism at the molecular level. A surge of recent experimentation indicates that STIM molecules function as Ca2+ sensors within the ER that, upon Ca2+ store depletion, rearrange to sites very near to the plasma membrane. At these plasma membrane-ER junctions, STIM interacts with and activates SOCE channels of the Orai family. The molecular and biophysical data that have led to these findings are discussed in this review, as are several controversies within this rapidly expanding field.
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