期刊
CHANNELS
卷 3, 期 4, 页码 221-225出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/chan.3.4.9198
关键词
TRPC channels; STIM1; SOCs; gating; electrostatic interaction
资金
- NHLBI NIH HHS [R00 HL093297, K99 HL093297] Funding Source: Medline
- NIDA NIH HHS [DA00266, DA10309] Funding Source: Medline
- NIDCR NIH HHS [DE12309] Funding Source: Medline
- NIDDK NIH HHS [DK38938] Funding Source: Medline
- NIMH NIH HHS [MH068830] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K99HL093297, R00HL093297] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R01DE012309] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK038938] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH068830] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA010309, R37DA010309, P50DA000266] Funding Source: NIH RePORTER
Store-operated Ca2+ channels (SOCs) are Ca2+ influx channels at the plasma membrane whose opening is determined by the level of Ca2+ stored in the endoplasmic reticulum lumen. SOCs are activated in response to receptor-mediated or passive depletion of ER Ca2+ to regulate many Ca2+-dependent cellular functions. Early work implicated the TRPC channels as SOCs. More recently, it was found that the Orai channels mediate the CRAC current and that the Ca2+ binding protein STIM1 functions as the ER Ca2+ sensor that mediates activation of the SOCs in response to depletion of ER Ca2+. Key questions are whether both TRPC and Orai channels are opened by STIM1 and the molecular mechanism by which STIM1 opens the SOCs. Ample biochemical and functional evidence indicate interaction of the TRPC channels with STIM1. Furthermore, it was found that STIM1 gates TRPC channels by electrostatic interaction of STIM1(K684,K685) in the polybasic domain of STIM1 with two negative charges (aspartates or glutamates) that are conserved in all TRPC channels. Charge mutants of STIM1(K684,K685)and TRPC1(D639,D640) and TRPC3(D697,D698) were used to develop further direct evidence for the function of TRPC channels as SOCs. The evidence in favor of TRPC channels as SOCs are discussed. Introduction
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