Andrew P. Somlyo

TL;DR: It is suggested that the RhoA/ROK pathway is constitutively active in a number of organs under physiological conditions; its aberrations play major roles in several disease states, particularly impacting on Ca2+ sensitization of smooth muscle in hypertension and possibly asthma and on cancer neoangiogenesis and cancer progression.

TL;DR: Abnormalities of these regulatory mechanisms and isoform variations may contribute to diseases of smooth muscle, and the G-protein-coupled inhibition of protein phosphatase is also likely to be impor-tant in regulating non-muscle cell functions mediated by cytoplasmic myosin II.

TL;DR: The results of these studies indicate that in SMC, RhoA-dependent regulation of the actin cytoskeleton selectively regulates SMC differentiation marker gene expression by modulating SRF-dependent transcription and suggest that RHoA signaling may serve as a convergence point for the multiple signaling pathways that regulate SMC differentiate.

TL;DR: It is shown that in smooth muscle permeabilized with beta-escin, one of the saponin esters, alpha 1-adrenergic and muscarinic agonists, as well as caffeine and InsP3, cause contractions mediated by Ca2+ release, which supports the conclusion that InsP 3 is the major physiological messenger of the Ca 2+ release component of pharmacomechanical coupling.

TL;DR: The hypothesis that the G-protein coupled Ca2(+)-sensitizing effect of agonists on force development is secondary to increased MLC20 phosphorylation is supported.