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When hormones, neurotransmitters or growth factors activate calcium signaling through the formation of inositol 1,4,5-trisphosphate (IP3), the rise in intracellular calcium ([Ca2+]i) is typically biphasic. The initial rise results from a direct effect of IP3 on the ligand-activated calcium channels in intracellular Ca2+-storing organelles. This release of intracellular Ca2+ is transient in nature and is usually followed by a more sustained elevation of the intracellular Ca2+ concentration ([Ca2+]i) due to Ca2+ entry across the plasma membrane. The predominant mechanism by which phospholipase C-coupled receptors activate Ca2+ entry is an indirect one. Ca2+ entry across the plasma membrane is coupled to the IP3-mediated depletion of intracellular Ca2+ stores, a process termed capacitative calcium entry or store-operated calcium entry (SOCE). In the past few years, the major molecular players in SOCE have been revealed: STIM1 and 2 which function as sensors for the Ca2+ level in the ER, and Orai1, 2 and 3 which are the pore-forming subunits of the SOC channel. Much of our work focuses on understanding the function and regulation of SOCE, especially in the context of these molecular entities.
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Alexander J Stevenson, Gilles Vanwalleghem,Teneale A Stewart,Nicholas D Condon, Bethan Lloyd-Lewis,Natascia Marino,James W Putney, Ethan K Scott, Adam D Ewing,Felicity M Davis
Proceedings of the National Academy of Sciences of the United States of Americano. 43 (2020): 26822-26832
NATURE COMMUNICATIONSno. 1 (2019): 1971-1971
Calcium Entry Channels in Non-Excitable Cellspp.311-324, (2017)
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