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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Regulation of Ca2+ release-activated Ca2+ channels by INAD and Ca2+ influx factor.

The coupling mechanism between depletion of Ca(2+) stores in the endoplasmic reticulum and plasma membrane store-operated ion channels is fundamental to Ca(2+) signaling in many cell types and has yet to be completely elucidated. Using Ca(2+) release-activated Ca(2+) (CRAC) channels in RBL-2H3 cells as a model system, we have shown that CRAC channels are maintained in the closed state by an inhibitory factor rather than being opened by the inositol 1,4,5-trisphosphate receptor. This inhibitory role can be fulfilled by the Drosophila protein INAD (inactivation-no after potential D). The action of INAD requires Ca(2+) and can be reversed by a diffusible Ca(2+) influx factor. Thus the coupling between the depletion of Ca(2+) stores and the activation of CRAC channels may involve a mammalian homologue of INAD and a low-molecular-weight, diffusible store-depletion signal.[1]


  1. Regulation of Ca2+ release-activated Ca2+ channels by INAD and Ca2+ influx factor. Su, Z., Barker, D.S., Csutora, P., Chang, T., Shoemaker, R.L., Marchase, R.B., Blalock, J.E. Am. J. Physiol., Cell Physiol. (2003) [Pubmed]
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