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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 (show RHOC Proteins)) 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 (show ROCK1 Proteins) pathway activated by excessive ROS (show ROS1 Proteins) is responsible for profilin-1 (show PFN1 Proteins)-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 (show WNT5A Proteins)-induced glioblastoma cell invasion.
PCGEM1 may be an inducer in epithelial ovarian cancer tumorigenesis and progression by upregulating RhoA and the subsequent expression of YAP (show YAP1 Proteins), P70S6K (show RPS6KB1 Proteins), MMP2 (show MMP2 Proteins), and Bcl-xL (show BCL2L1 Proteins).
This study identified Piezo2 mechanosensitive cationic channel as a transducer of environmental physical cues into mechanobiological responses.
High RHOA expression is associated with gastric cancer invasion and metastasis.
Non-visual arrestins regulate the focal adhesion formation via small GTPases RhoA and Rac1 independently of G-protein-coupled receptors.
RHOA loss reduces YAP (show YAP1 Proteins) signaling of the Hippo pathway and affects YAP (show YAP1 Proteins) effector epiregulin (EREG (show EREG Proteins)) expression in the crypts. Expression of an active YAP (show YAP1 Proteins) (S112A) mutant rescues ntestinal stem cells (ISCs (show NFS1 Proteins)) marker expression, ISC regeneration, and ISC-associated Wnt (show WNT2 Proteins) signaling, but not defective epithelial polarity, in RhoA knockout mice, implicating YAP (show YAP1 Proteins) in RHOA-regulated ISC function.
GTP (show AK3 Proteins)-RhoA and ROCK1 (show ROCK1 Proteins) 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 (show NFKB1 Proteins).
RhoA modulates the choices of molar cuspal shape by coordinating adhesion junctions, actin distribution, and fibronectin (show FN1 Proteins) 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.
These results reveal a novel signaling network, the Sema4D (show SEMA4D Proteins)-RhoA-Akt (show AKT1 Proteins) signal cascade, that coordinates cellular function and morphology and highlights the importance of specific spatiotemporally restricted components of a signaling pathway in the regulation of ameloblast differentiation.
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 (show EGFL7 Proteins)/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 (show KAZ Proteins) interacts with ARVCF (show ARVCF Proteins)-catenin, spectrin and p190B RhoGAP (show ARHGAP1 Proteins), 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 (show SRC Proteins)/FAK (show PTK2 Proteins) activation in response to shear stress.
the Lbc/alpha-catulin (show CTNNAL1 Proteins) axis participates in 5-HT (show DDC Proteins)-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 (show PTK2 Proteins)-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 (show CA2 Proteins)+)](i), as well as the voltage-dependent Ca(2 (show CA2 Proteins)+) currents
the Rho-ROCK signal pathway contributes to VEGF (show VEGFA Proteins)-induced hyperpermeability. Myosin light-chain phosphorylation and actin stress fiber formation occur concomitantly with the increase in permeability upon VEGF (show VEGFA Proteins) stimulation.
Formation of polygonal actin network in endothelial cells is a novel rhoA associated response to hypertonic stress.
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 (show PTK2 Proteins) phosphorylation, thereby activating cell proliferation and migration in bovine aortic endothelial cells.
Pseudorabies virus US3 expression led to RhoA phosphorylation at serine 188 to induce actin rearrangements.
Data indicate that TNF-alpha (show TNF Proteins) stimulates Rac (show AKT1 Proteins), ADAM17/TACE (show ADAM17 Proteins), and RhoA through the guanine nucleotide exchange factor (show ARHGEF12 Proteins) (GEF)-H1 (show ARHGEF2 Proteins).
Contractile pulmonary arterial myocytes exhibit marked Rho-dependent actin polymerization in hypoxia, with increased active RhoA and LIMK (show LIMK1 Proteins) phosphorylation.
Results suggest that Rac1 and RhoA are regulated by TGFbeta1 (show TGFB1 Proteins) 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 (show ROCK1 Proteins) 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