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Inhibition of hormone-induced Ca2+ release from intracellular stores by cGMP involves a protein complex which consists of at least 3 proteins, i.e. the inositol-1,3,4-phosphat receptor (IP3R), the cGMP-dependent protein kinase (cGK), and, as a linker protein between both, the inositol1,3,4-phosphat receptor associated G-kinase substrate (IRAG [1]). Recently, mutant mice were created which lack the part of the IRAG protein that is supposed to mediate the association between IRAG and the IP3R. In these mice (IRAG∆12 mice), cGMP failed to attenuate both, hormone-induced Ca2+ signals and hormone-induced contractions in vascular preparations [2]. These result confirm the concept that IRAG is an essential mediator of relaxation mediated by cGMP/cGK signalling in vascular smooth muscle.

IRAG is involved in cGMP/cGK-mediated relaxation of contractions induced by calcium entry