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Rho-associated, coiled-coil containing protein kinase 1

Rho kinase
This gene encodes a protein serine/threonine kinase that is activated when bound to the GTP-bound form of Rho. The small GTPase Rho regulates formation of focal adhesions and stress fibers of fibroblasts, as well as adhesion and aggregation of platelets and lymphocytes by shuttling between the inactive GDP-bound form and the active GTP-bound form. Rho is also essential in cytokinesis and plays a role in transcriptional activation by serum response factor. This protein, a downstream effector of Rho, phosphorylates and activates LIM kinase, which in turn, phosphorylates cofilin, inhibiting its actin-depolymerizing activity. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Rhodopsin, RhoA, V1a, Actin, CAN
Papers using Rho kinase antibodies
Good manufacturing practice and clinical-grade human embryonic stem cell lines
Hovatta Outi et al., In In Vitro Cellular & Developmental Biology. Animal, 2007
... Culture form single cell suspension has been feasible using a Rho-kinase inhibitor Y-27632, (Merck Chemicals Ltd., Nottingham, UK; ...
Integrin transmembrane signaling and cytoskeletal control
Holly Jeff M. P. et al., In Frontiers in Endocrinology, 1994
... The Rho kinase inhibitor ROCK, Y-27632, and C2-ceramide were purchased from Merck, Nottingham, UK ...
Papers on Rho kinase
Changes of synapses in experimental autoimmune encephalomyelitis by using Fasudil.
Xiao et al., Datong, China. In Wound Repair Regen, Feb 2016
Fasudil ameliorated the clinical severity of EAE and inhibited Rho kinase (ROCK), especially ROCK II, in brain and spinal cord of EAE mice.
Development of Bipotent Cardiac/Skeletal Myogenic Progenitors from MESP1+ Mesoderm.
Kyba et al., Minneapolis, United States. In Stem Cell Reports, Feb 2016
Using this system, we investigate the regulation of these bipotent progenitors, and find that cardiac specification is governed by an antagonistic TGFβ-BMP axis, while skeletal muscle specification is enhanced by Rho kinase inhibition.
Effects of glucagon-like peptide-1 on advanced glycation endproduct-induced aortic endothelial dysfunction in streptozotocin-induced diabetic rats: possible roles of Rho kinase- and AMP kinase-mediated nuclear factor κB signaling pathways.
Wang et al., Hefei, China. In Endocrine, Feb 2016
UNASSIGNED: Interaction between advanced glycation endproducts (AGEs) and receptor for AGEs (RAGE) as well as downstream pathways leads to vascular endothelial dysfunction in diabetes.
G protein-coupled receptors: signalling and regulation by lipid agonists for improved glucose homoeostasis.
McKillop et al., Coleraine, United Kingdom. In Acta Diabetol, Feb 2016
In addition, GPR43 also couples to the Gαq subunit augmenting intracellular Ca(2+) and activating phospholipase C. GPR55 is specific for cannabinoid endogenous agonists (endocannabinoids) and non-cannabinoid fatty acids, which couples to Gα12/13 and Gαq proteins, leading to enhancing intracellular Ca(2+), extracellular signal-regulated kinase 1/2 (ERK) phosphorylation and Rho kinase.
Differential regulation of endothelial nitric oxide synthase phosphorylation by protease-activated receptors in adult human endothelial cells.
Motley et al., Nashville, United States. In Exp Biol Med (maywood), Feb 2016
In addition, we confirmed that PAR-mediated eNOS-Ser-1177 phosphorylation was Ca(2+)-dependent using the Ca(2+) chelator, BAPTA, while eNOS-Thr-495 phosphorylation was mediated via Rho kinase using the ROCK inhibitor, Y-27632, suggesting protease-activated receptor coupling to Gq and G12/13, respectively.
Microparticles generated during chronic cerebral ischemia increase the permeability of microvascular endothelial barriers in vitro.
Thompson et al., Ottawa, Canada. In Brain Res, Jan 2016
The reduction in TEER was attenuated by treating endothelial barriers prior to exposure to MPs with the caspase 3 inhibitor AC-DEVD-CHO, the TNF-α inhibitor SPD304, the tumor necrosis factor alpha-converting enzyme (TACE, ADAM 17) inhibitor TAPI-0-1 and the Rho kinase (ROCK) inhibitor Y-27632, and by treating the MPs themselves with these inhibitors prior to applying them to cultured cells.
Ozone-induced airway hyperresponsiveness: roles of ROCK isoforms.
Song et al., Birmingham, United States. In Am J Physiol Lung Cell Mol Physiol, Jan 2016
Compared with wild-type (WT) mice, the authors report that ROCK1(+/-) and ROCK2(+/-) mice exhibited significantly reduced AHR following acute exposure to O3.
Rho kinase inhibitors for glaucoma treatment - Review.
Susanna Junior et al., São Paulo, Brazil. In Arq Bras Oftalmol, Dec 2015
Currently, an increasing number of researches involve Rho kinase inhibitors, which are a new pharmacological class of hypotensive agents specifically targeting the diseased trabecular outflow pathway.
Cdk1-dependent mitotic enrichment of cortical myosin II promotes cell rounding against confinement.
Muller et al., Basel, Switzerland. In Nat Cell Biol, Feb 2015
Our data suggest that progressive accumulation of myosin II to the mitotic cell cortex probably requires the Cdk1 activation of both p21-activated kinases, which inhibit myosin recruitment, and of Rho kinase, which stimulates myosin recruitment to the cortex.
Novel Therapeutic Strategies for Reducing Right Heart Failure Associated Mortality in Fibrotic Lung Diseases.
Oyenuga et al., Chicago, United States. In Biomed Res Int, 2014
Specific therapies targeting pulmonary hypertension include calcium channel blockers, endothelin (ET-1) receptor antagonists, prostacyclin analogs, phosphodiesterase type 5 (PDE5) inhibitors, and rho-kinase (ROCK) inhibitors.
Rho kinase inhibitor AMA0526 improves surgical outcome in a rabbit model of glaucoma filtration surgery.
Stalmans et al., Leuven, Belgium. In Prog Brain Res, 2014
PURPOSE: First, to elucidate the effect of Rho kinase inhibitor, AMA0526, on Human Tenon Fibroblast (HTF) proliferation and transdifferentiation to myofibroblasts.
Vascular RhoJ is an effective and selective target for tumor angiogenesis and vascular disruption.
Koh et al., South Korea. In Cancer Cell, 2014
RhoJ blockade provides a double assault on tumor vessels by both inhibiting tumor angiogenesis and disrupting the preformed tumor vessels through the activation of the RhoA-ROCK (Rho kinase) signaling pathway in tumor endothelial cells, consequently resulting in a functional failure of tumor vasculatures.
PPAR-ϒ pathway to vascular dysfunction.
Cowley et al., Milwaukee, United States. In Cell Metab, 2012
(2012) shows that loss of PPAR-ϒ repression of the Rho kinase pathway leads to altered vascular function via a smooth-muscle-dependent pathway that is independent of NO and oxidant stress.
Regulation of the actin cytoskeleton by Rho kinase controls antigen presentation by CD1d.
Brutkiewicz et al., Indianapolis, United States. In J Immunol, 2012
our overall results reveal a model whereby CD1d-mediated Ag presentation is negatively regulated by ROCK1 and ROCK2 via its effects on the actin cytoskeleton.
Molecular mechanisms regulating the vascular prostacyclin pathways and their adaptation during pregnancy and in the newborn.
Khalil et al., Boston, United States. In Pharmacol Rev, 2012
PGI(2)/IP interaction stimulates G protein-coupled increase in cAMP and protein kinase A, resulting in decreased [Ca(2+)](i), and could also cause inhibition of Rho kinase, leading to vascular smooth muscle relaxation.
Novel mechanism for negatively regulating Rho-kinase (ROCK) signaling through Coronin1B protein in neuregulin 1 (NRG-1)-induced tumor cell motility.
Worthylake et al., New Orleans, United States. In J Biol Chem, 2012
analysis of the mechanism for negatively regulating Rho-kinase (ROCK) signaling through Coronin1B protein in neuregulin 1 (NRG-1)-induced tumor cell motility
Structure of Shroom domain 2 reveals a three-segmented coiled-coil required for dimerization, Rock binding, and apical constriction.
VanDemark et al., Pittsburgh, United States. In Mol Biol Cell, 2012
The structure of Shrm domain 2 (SD2), which mediates the interaction with Rock and is required for Shrm function, is reported.
Planar cell polarity links axes of spatial dynamics in neural-tube closure.
Takeichi et al., Kōbe, Japan. In Cell, 2012
At these AJs, Celsr1 cooperates with Dishevelled, DAAM1, and the PDZ-RhoGEF to upregulate Rho kinase, causing their actomyosin-dependent contraction in a planar-polarized manner.
Regulation of glucose transport by ROCK1 differs from that of ROCK2 and is controlled by actin polymerization.
Kim et al., Boston, United States. In Endocrinology, 2012
Regulation of glucose transport by ROCK1 differs from that of ROCK2 and is controlled by actin polymerization.
Matrix-bound PAI-1 supports cell blebbing via RhoA/ROCK1 signaling.
Barlovatz-Meimon et al., France. In Plos One, 2011
Matrix-associated PAI-1 plays a role in the cell behavior needed for amoeboid migration by maintaining cell blebbing, localizing PDK1 and ROCK1 at the cell membrane and maintaining the RhoA/ROCK1/MLC-P pathway activation.
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