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the RhoA antagonist, SRGAP1, is present at subconfluent junctions to a greater extent than in confluent cultures and SRGAP1 RNAi restores RhoA signaling and contractility in subconfluent cultures to levels seen in confluent cells.
High RHOA expression is associated with asthmatic airway hyper-responsiveness.
Strain also mediated myofibroblast differentiation via the RhoA/ROCK2-MRTF-A/SRF pathway. These findings provided evidence for a mechanical strain-induced RhoA/ROCK2 pathway that may contribute to myopia scleral remodeling.
Loss of RhoA promotes skin tumor formation and invasion.
Interplay of cell-cell contacts and RhoA/MRTF-A signaling regulates cardiomyocyte identity.
Study in squamous cell carcinoma (SCC) cells and tissues findings demonstrate the tumor suppressor role of miR-340 in SCC by directly regulating RhoA.
results highlight a role for the C-terminal 15 amino acids in the membrane association of TGAT and the subsequent activation of RhoA and actin polymerization by TGAT
Phospho-VAV1 staining was demonstrated in the clinical specimens harboring G17V RHOA and VAV1 mutations at a higher frequency than those without. Our findings indicate that the G17V RHOA-VAV1 axis may provide a new therapeutic target in AITL.
Study report that galectin3 expression is upregulated in nonsmall cell lung cancer cells under hypoxia and that it contributes to tumor cell migration and invasion. Cell motility is upregulated by the function of activated RhoA, which is induced by high levels of cytoplasmic galectin3.
Ezrin interacts with MYOGEF and recruits it to retracting blebs, where MYOGEF activates RhoA and promotes the reassembly of the cortical actomyosin network at the bleb membrane, thus contributing to the regulation of bleb retraction.
This study solved the structure of a RhoA/Net1 heterodimer with X-ray crystallography at 2-A resolution.
Results found complex pattern of inactivation of RHOA in colon cancer cells (CRC) involving overlapping genetic, transcriptional and post-transcriptional mechanisms. Deletions affecting RHOA are associated with its reduced expression which regulated by miR-200a/b/429. In addition, RHOA is regulated by SMAD4 and c-MYC, key mediators of the most commonly deregulated signaling pathways in CRC TGF-b and Wnt respectively.
The results suggest that human parainfluenza virus type 2 (hPIV-2) V protein enhances hPIV2 growth through RhoA-induced F-actin formation, by selectively binding to inactive RhoA.
This article summarizes recent progress on the mechanisms that control the expression of the three members of the Rho-like subfamily (RhoA, RhoB, and RhoC) at the level of gene transcription as well as their post-transcriptional regulation by microRNAs. [review]
Overexpression of miR133b inhibited the proliferation and promoted apoptosis in a diabetic retinopathy cell model by downregulating RhoA expression.
silencing of URG11 altered the expression levels of cell cycleassociated genes, epithelialmesenchymal transitionassociated genes, and RhoA and ROCK1 protein levels. Thus, the results of the present study suggest that URG11 may be a potential therapeutic target, which may be important to inhibit the development and progression of prostatic hyperplasia.
Results suggested that the RhoA/ROCK1 pathway activated by excessive ROS is responsible for profilin-1-mediated endothelial damage.
We found that lipid radicals govern changes in podocyte homeostasis through redox sensitive RhoA signaling: lipid radicals inhibit migration and cause loss of F-actin fibers. These effects were prevented by mutating the redox sensitive cysteines of RhoA.
Data show that p120-catenin interacts with kinesin family member 23 (MKLP1) to regulate focused rhoA GTP-binding protein (RhoA) activity during cytokinesis.
Data show that RhoA is upregulated in invasive glioblastoma tissues, and its activation participates in Wnt5a-induced glioblastoma cell invasion.
mechanical activation of RhoA in mesenchymal progenitors is dependent on LARG, while ARHGAP18 limits RhoA delineated cytoskeletal structure in static cultures
In addition to enhanced RhoA-mediated Ca(2+) sensitization following CH, RhoA can also activate a Ca(2+) signal by facilitating ASIC1a plasma membrane localization and Ca(2+) influx in pulmonary hypertension.
Trio induces RhoA activation downstream of Slit2, and support a functional role in ensuring the proper positioning of both guidepost cells and a major axonal tract.
Study demonstrates that the non-canonical SMO/Gi/RHOA pathway functions outside primary cilia: Kif3a-deficient fibroblasts, unable to form primary cilia and to activate the canonical Hedgehog pathway, can activate RHOA robustly after stimulation of endogenous SMO with SHH or purmorphamine, and that KIF3A re-expression rescues ciliogenesis but does not affect RHOA activation.
These findings elucidated the molecular mechanism of anti-freezing, involving RhoA phosphorylation, meditated by the Rho/ROCK signalling pathway, in hatched and diapaused murine blastocysts.
Stat3 controls reactive astrocyte dynamics with a critical role for RhoA, a key regulator of actin dynamics.
This study observed impaired collagen I secretion in mesenchymal stem cells lacking RhoA or Cdc42.
RhoA activation results in actin stress fibre formation, growth cone collapse, and impaired axonal transport
KLF4 indirectly modulates the actin cytoskeleton morphology via activity of RhoA in order to inhibit cellular migration and invasion.
Cdc42 and RhoA act as a regulatory circuit downstream of the megakaryocytes -specific mechanoreceptor GPIb to coordinate polarized transendothelial platelet biogenesis.
Non-visual arrestins regulate the focal adhesion formation via small GTPases RhoA and Rac1 independently of G-protein-coupled receptors.
RHOA loss reduces YAP signaling of the Hippo pathway and affects YAP effector epiregulin (EREG) expression in the crypts. Expression of an active YAP (S112A) mutant rescues ntestinal stem cells (ISCs) marker expression, ISC regeneration, and ISC-associated Wnt signaling, but not defective epithelial polarity, in RhoA knockout mice, implicating YAP in RHOA-regulated ISC function.
GTP-RhoA and ROCK1 expression levels were markedly increased in a time-dependent manner in the ears and lungs of mice treated with penicillin.
Tyr42 phosphorylation of RhoA GTPase promotes tumorigenesis through NF-kappaB.
RhoA modulates the choices of molar cuspal shape by coordinating adhesion junctions, actin distribution, and fibronectin localization to drive inner dental epithelium invagination.
Kctd13 deletion reduces synaptic transmission, which correlates with increased levels of RhoA, a KCTD13/CUL3 ubiquitin ligase substrate
Crmp4(-/-) OBs exhibited enhanced activation of RhoA/focal adhesion kinase (FAK) signaling that led to cytoskeletal changes with increased cell spreading.
Codepletion of the actomyosin regulator RhoA and Afadin results in defects in the central lumens and arrests lumen remodeling
Hydrogen peroxide oxidizes RhoA at Cys16 and Cys20, and activates RhoA via Vav2.
Mgc's GAP activity down-regulates the active populations of RhoA and Rac1 at localized regions of epithelial cells and is necessary for successful cytokinesis and cell-cell junction structure
Data show that shortly after anaphase onset oocytes and embryonic cells exhibit cortical waves of Rho activity and F-actin polymerization.
CASZ1/Egfl7/RhoA pathway is necessary for promoting endothelial cell behaviors associated with proper vascular assembly.
RhoA can be considered a component of the intracellular pattern formation system.
Kazrin interacts with ARVCF-catenin, spectrin and p190B RhoGAP, and modulates RhoA activity.
Morphogenesis of the primitive gut tube is generated by Rho/ROCK/myosin II-mediated endoderm rearrangements.
RhoA and membrane fluidity mediates the spatially polarized Src/FAK activation in response to shear stress.
This work provides the first evidence of a global signaling event in response to a localized mechanical stress.
the Lbc/alpha-catulin axis participates in 5-HT-induced PASMC mitogenesis and RhoA/ROCK signaling, and may be an interventional target in diseases involving vascular smooth muscle remodeling.
The RhoA/ROCK signaling pathway is an important negative regulator of vascular calcification.
Vascular endothelial-cadherin signals through RhoA and actin cytoskeletal and affects cell-matrix adhesion
Thrombospondin has a role in inducing RhoA inactivation through FAK-dependent signaling to stimulate focal adhesion disassembly
KCl directly increased Rho and ROCK activities in a concentration-dependent fashion that paralleled closely the effect of KCl on lung smooth muscle tone and [Ca(2+)](i), as well as the voltage-dependent Ca(2+) currents
the Rho-ROCK signal pathway contributes to VEGF-induced hyperpermeability. Myosin light-chain phosphorylation and actin stress fiber formation occur concomitantly with the increase in permeability upon VEGF stimulation.
Formation of polygonal actin network in endothelial cells is a novel rhoA associated response to hypertonic stress.
These results suggest the existence of a feedback loop between cytoskeletal tension, adhesion maturation, and ROCK signaling that likely contributes to numerous mechanochemical processes.
Cadherins, RhoA and Rac1, have important roles in mechanotransduction and that endothelial and smooth muscle cells use different mechanisms to respond to stretch.
Results indicate that hypergravity induces ATP release and actin reorganization via RhoA activation and FAK phosphorylation, thereby activating cell proliferation and migration in bovine aortic endothelial cells.
In all, these results demonstrate that cell-cell contact signals through VE-cadherin, RhoA, and intracellular tension in the actin cytoskeleton to regulate proliferation.
These results demonstrate the critical role of the RhoA/alphavbeta5 integrin pathway in mediating Pseudomonas aeruginosa-induced lung vascular permeability.
A functional contribution of PI3K, Rho, and ROCK to both the autocrine mechanism of ATP release and ATP-mediated angiogenic activation of vasa vasorum endothelial cells, is reported.
Pseudorabies virus US3 expression led to RhoA phosphorylation at serine 188 to induce actin rearrangements.
Data indicate that TNF-alpha stimulates Rac, ADAM17/TACE, and RhoA through the guanine nucleotide exchange factor (GEF)-H1.
Contractile pulmonary arterial myocytes exhibit marked Rho-dependent actin polymerization in hypoxia, with increased active RhoA and LIMK phosphorylation.
Results suggest that Rac1 and RhoA are regulated by TGFbeta1 in the process of endothelial tube formation in collagen I gels.
The concentration of RhoA mRNA and activated RhoA enzyme were greater in urothelium than in detrusor. Rho kinase inhibitor Y-27632 showed a stronger inhibitory effect in detrusor with intact urothelium.
Thrombin stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1, RhoA, and myocardin.
Activating Rho could be beneficial to suppress Kras mutant-induced liver malignancies.
Regulates a signal transduction pathway linking plasma membrane receptors to the assembly of focal adhesions and actin stress fibers. Involved in a microtubule-dependent signal that is required for the myosin contractile ring formation during cell cycle cytokinesis. Plays an essential role in cleavage furrow formation. Required for the apical junction formation of keratinocyte cell-cell adhesion. Serves as a target for the yopT cysteine peptidase from Yersinia pestis, vector of the plague, and Yersinia pseudotuberculosis, which causes gastrointestinal disorders. Stimulates PKN2 kinase activity. May be an activator of PLCE1. Activated by ARHGEF2, which promotes the exchange of GDP for GTP. Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly. The MEMO1-RHOA- DIAPH1 signaling pathway plays an important role in ERBB2- dependent stabilization of microtubules at the cell cortex. It controls the localization of APC and CLASP2 to the cell membrane, via the regulation of GSK3B activity. In turn, membrane-bound APC allows the localization of the MACF1 to the cell membrane, which is required for microtubule capture and stabilization.
Aplysia ras-related homolog 12
, oncogene RHO H12
, ras homolog gene family, member A
, rho cDNA clone 12
, small GTP binding protein RhoA
, transforming protein RhoA
, Ras family member A
, Rho family GTPase
, aplysia ras-related homolog A
, aplysia ras-related homolog A1
, aplysia ras-related homolog A2
, ras homolog A1
, ras homolog A2
, ras homolog gene family, member A1
, ras homolog gene family, member A2
, plysia ras-related homolog A2
, rho1 GTP-binding protein
, RhoA GTPase
, Rho A