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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAQb4CVEPvFjoBWsQTjJKApr2vsTiukfuufYa6ujgb1Bs#_9 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAQb4CVEPvFjoBWsQTjJKApr2vsTiukfuufYa6ujgb1Bs#_8 http://www.w3.org/ns/prov#value FIG. 11. Proposed mechanism of regulation of smooth muscle contraction via inhibition of MLCP via the RhoA/ROK pathway and phosphorylation of myosin by ILK. Contractile agonists such as endothelin-1, angiotensin II, and vasopressin act via receptors that are coupled to both Gq/11 and G12/13 heterotrimeric G proteins (43). Gq/11 activates phospholipase Cb (PLCb), which hydrolyzes phosphatidylinositol 4,5- bisphosphate (PIP2) to generate inositol 1,4,5-trisphosphate (IP3) and 1,2-diacylglycerol. Inositol 1,4,5-trisphosphate diffuses to the sarcoplasmic reticulum (SR), where it interacts with the inositol 1,4,5-trisphosphate receptor, a Ca21 release channel in the sarcoplasmic reticulum membrane, thereby triggering Ca21 release from the sarcoplasmic reticulum. 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