期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1865, 期 3, 页码 463-469出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2017.12.001
关键词
STIM1; Orai1; SARAF; Store-operated calcium entry; Slow Ca2+-dependent inactivation
资金
- MINECO [BFU2013-45564-C2-1-P, BFU2016-74932-C2-1-P]
- Junta de Extremadura-FEDER [IB16046, GR15029]
- Juan de la Cierva Program [JCI_2012-12934, IJCI_2015-25665]
Store-operated Ca2+ entry (SOCE) is a functionally relevant mechanism for Ca2+ influx present in electrically excitable and non-excitable cells. Regulation of Ca2+ entry through store-operated channels is essential to maintain an appropriate intracellular Ca2+ homeostasis and prevent cell damage. Calcium-release activated channels exhibit Ca2+-dependent inactivation mediated by two temporally separated mechanisms: fast Ca2+-dependent inactivation takes effect in the order of milliseconds and involves the interaction of Ca2+ with residues in the channel pore while slow Ca2+-dependent inactivation (SCDI) develops over tens of seconds, requires a global rise in [Ca2+](cyt) and is a mechanism regulated by mitochondria. Recent studies have provided evidence that the protein SARAF (SOCE-associated regulatory factor) is involved in the mechanism underlying SCDI of Orail. SARAF is an endoplasmic reticulum (ER) membrane protein that associates with STIM1 and translocate to plasma membrane-ER junctions in a STIM1-dependent manner upon store depletion to modulate SOCE. SCDI mediated by SARAF depends on the location of the STIM1-Orail complex within a PI(4,5)P2-rich microdomain. SARAF also interacts with Orail and TRPC1 in cells endogenously expressing STIM1 and cells with a low STIM1 expression and modulates channel function. This review focuses on the modulation by SARAF of SOCE and other forms of Ca2+ influx mediated by Orail and TRPC1 in order to provide spatio-temporally regulated Ca2+ signals.
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