ROCK1

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ROCK1

A gene on chromosome 18q11.1 that encodes a protein kinase, which is a key regulator of actin cytoskeleton and cell polarity. It regulates smooth muscle contraction, actin cytoskeleton organisation, stress-fibre and focal adhesion formation, and neurite retraction, as well as cell adhesion and motility via phosphorylation of DAPK3, GFAP, LIMK1, LIMK2, MYL9/MLC2, PFN1 and PPP1R12A. It phosphorylates FHOD1, and both promote SRC-dependent non-apoptotic plasma membrane blebbing. ROCK1 also: phosphorylates JIP3 and regulates JNK to JIP3 recruitment in response to UVB-induced stress; suppresses inflammatory cell migration by regulating PTEN phosphorylation and stability; downregulates VEGF-induced angiogenic endothelial cell activation; promotes keratinocyte terminal differentiation; and plays a role in terminal erythroid differentiation. ROCK1 is required for centrosome positioning and centrosome-dependent exit from mitosis. It may regulate closure of the eyelids and ventral body wall by inducing the assembly of actomyosin bundles.
References in periodicals archive ?
(2007) Rho kinase contributes to basal vascular tone in humans: Role of endothelium-derived nitric oxide.
Ueno et al., "The new therapeutic concept of using a rho kinase inhibitor for the treatment of corneal endothelial dysfunction," Cornea, vol.
van Hinsbergh, "Role of RhoA and Rho kinase in lysophosphatidic acid-induced endothelial barrier dysfunction," Arteriosclerosis, Thrombosis, and Vascular Biology, vol.
The Rho kinase pathway can also be activated by a variety of factors such as Thromboxane A2, Angiotensin II, Thrombin, Wnt, Endothelin-1, extracellular matrix, and stretch [64].
In conjunction, the company's preclinical studies have demonstrated that Rhopressa lowers episcleral venous pressure, which contributes half of IOP in healthy subjects; provides an additional mechanism that reduces fluid production in the eye and lowers IOP; inhibits both Rho Kinase (ROCK) and norepinephrine transporter (NET); As well as may have an anti-fibrotic effect on the trabecular meshwork and the potential to increase perfusion of the trabecular meshwork.
AR-13154 targets Rho Kinase, Janus Kinase 2, and platelet-derived growth factor receptor beta.
Adenosine receptor agonists are showing promise in early phase trials for glaucoma, while Rho kinase (ROCK) inhibitors, which target the trabecular meshwork, continue to work their way through the development pipeline.
Rho kinase has been shown to phosphorylate MYPT-1 at [Thr.sup.695], which decreases its phosphatase activity (6), leading to increases in MLC phosphorylation and force development (7).
Second, MLCP is also negatively controlled by RhoA and its target Rho Kinase, which deactivates MLCP similarly through phosphorylation.
ET-1 induces SphK1 and Rho kinase through [Ca.sup.2+] sensitization which comprises an important mechanism in normal parturition [63].
For example, while Rho kinase (mainly ROCKII), glycogen synthase kinase-3[beta] (GSK-3[beta]), cyclin-dependent kinase-5 (Cdk5), and phosphatases are all essential for normal neuronal development [7], they may all be involved in a plethora of neurodegenerative disorders through a central pathogenic mechanism.
They had discovered that adding two different substances to these cells (a Rho kinase inhibitor and fibroblast feeder cells) pushes them to morph into stem-like cells that stay alive indefinitely.