SOCs and the IP3 Receptor

Science's STKE  07 Mar 2000:
Vol. 2000, Issue 22, pp. tw4
DOI: 10.1126/stke.2000.22.tw4

Many cell functions are regulated through changes in the concentration of intracellular free calcium ([Ca2+]I). Often, stimuli that cause release of Ca2+ from intracellular stores later cause influx of Ca2+ through channels in the plasma membrane. However, the identity of these so-called store-operated channels (SOCs) in the plasma membrane and the mechanisms by which they are coupled to emptying of intracellular stores has remained unclear. Ma et al. took advantage of a new inhibitor of inositol trisphosphate (IP3) receptors to show that the IP3 receptor channels (which mediate release of Ca2+ from intracellular stores) are required for both activation and maintained conductance of SOCs in the plasma membrane. The effects of the IP3 channel inhibitor are not the result of alterations in Ca2+ release. The results also distinguish the SOCs from TRP channels, which have been considered to be another candidate to mediate Ca2+ influx after depletion of intracellular stores.

Ma, H.-T., Patterson, R.L., Van Rossum, D.B., Birnbaumer, L., Mikoshiba, K., and Gill, D.L. (2000) Requirement of the inositol trisphosphate receptor for activation of store-operated Ca2+ channels. Science 287: 1647-1651. [Abstract] [Full Text]