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First published online 3 May 2007
doi: 10.1242/jcs.03462

Journal of Cell Science 120, 1959-1965 (2007)
Published by The Company of Biologists 2007
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New molecular players in capacitative Ca2+ entry

James W. Putney, Jr

National Institute of Environmental Health Sciences – NIH, PO Box 12233, Research Triangle Park, NC 27709, USA


Figure 1
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  		Fig. 1. The roles of Stim1 and Orai. Agonist (Ag) activation of a plasma membrane receptor (R) results in formation of Ins(1,4,5)P3, which activates the Ins(1,4,5)P3 receptor (IP3R) causing discharge of stored Ca2+ from a subcompartment of the endoplasmic reticulum. Within this subcompartment, Ca2+ binds reversibly to an EF hand motif in Stim1; depletion of Ca2+ results in dissociation of Ca2+ from Stim1, which causes Stim1 to redistribute within the endoplasmic reticulum to areas near Orai channels that reside in the plasma membrane. Stim1 then activates Ca2+-selective Orai channels; the mechanism by which this activation is accomplished is unknown at present. Stim1 is also present in the plasma membrane, although its function there is unclear. TRPC channels can also be activated by phospholipase C (PLC)-dependent mechanisms. There is evidence that in some instances, perhaps when combined with other subunits, they can function as store-operated channels, perhaps also involving Stim1 as an activator. Figure modified from Putney, 2007Go (Putney, 2007Go).

 

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© The Company of Biologists Ltd 2007