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anti-Human RHOA Antibodies:
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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 (show CASZ1 Antibodies)/Egfl7 (show EGFL7 Antibodies)/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 Antibodies) interacts with ARVCF (show ARVCF Antibodies)-catenin, spectrin and p190B (show ARHGAP5 Antibodies) RhoGAP (show ARHGAP1 Antibodies), and modulates RhoA activity.
Morphogenesis of the primitive gut tube is generated by Rho/ROCK/myosin II-mediated endoderm rearrangements.
TET2 (show TET2 Antibodies) and RhoA mutations cooperatively disrupt T cell homeostasis
Genetic variant in RhoA gene is associated with progression of prostate cancer.
Downregulation of Cul3 (show CUL3 Antibodies) led to a marked increase in RhoA protein expression after 6 days of adipocytes differentiation, suggesting that Cul3 (show CUL3 Antibodies) is involved in the regulation of RhoA stability.
High RHOA expression is associated with colon cancer cell migration.
P311 could accelerate skin wound reepithelialization by promoting the migration of Epidermal Stem Cell through RhoA and Rac1 activation.
Findings indicate a tumor suppressive role for G protein subunit alpha 13 (Galpha13 (show GNA13 Antibodies)) and rhoA GTP-binding protein (RhoA) in Burkitt's lymphoma and diffuse large B-cell lymphoma (DLBCL).
RhoA/ROCK and Raf-1 (show RAF1 Antibodies)/CK2 (show CSNK2A1 Antibodies) pathway are responsible for TNF-alpha (show TNF Antibodies)-mediated endothelial cytotoxicity via regulation of the vimentin (show VIM Antibodies) cytoskeleton.
Rac (show AKT1 Antibodies) is required to stimulate the remodeling of mast cells, triggering actin-mediated flattening of the cell periphery to create an active degranulation zone, whereas RhoA controls the streaming of highly motile granules into the active zone.
the use of N1-Guanyl (show GUCA2A Antibodies)-1,7-diaminoheptane, a DHPS (show DHPS Antibodies) inhibitor, resulted in a significant decrease in tumor formation in vivo. In patients with esophageal squamous cell carcinoma (ESCC), overexpression of DHPS (show DHPS Antibodies) in ESCC tumors was significantly associated with worse recurrence-free survival, and correlated with distant metastasis.
Besides controlling cyclin (show PCNA Antibodies)/CDK (show CDK4 Antibodies) kinase activity, p27 (show PAK2 Antibodies) also regulates cytoskeletal dynamics, cell motility and cell invasion. Following processing by caspases, p27 (show PAK2 Antibodies) fails to bind to RhoA and to inhibit its activation, and thereby abolishes the ability of p27 (show PAK2 Antibodies) to stimulate cell migration and invasion
Pseudorabies virus US3 expression led to RhoA phosphorylation at serine 188 to induce actin rearrangements.
Data indicate that TNF-alpha (show TNF Antibodies) stimulates Rac (show AKT1 Antibodies), ADAM17/TACE (show ADAM17 Antibodies), and RhoA through the guanine nucleotide exchange factor (show ARHGEF12 Antibodies) (GEF)-H1 (show ARHGEF2 Antibodies).
Contractile pulmonary arterial myocytes exhibit marked Rho-dependent actin polymerization in hypoxia, with increased active RhoA and LIMK (show LIMK1 Antibodies) phosphorylation.
Results suggest that Rac1 and RhoA are regulated by TGFbeta1 (show TGFB1 Antibodies) 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 Antibodies) inhibitor Y-27632 showed a stronger inhibitory effect in detrusor with intact urothelium.
Thrombin (show F2 Antibodies) stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1 (show F2R Antibodies), RhoA, and myocardin (show MYOCD Antibodies).
Data indicate that oxidative stress in diabetes causes a decrease in miR (show MLXIP Antibodies)-133a expression leading to an increase in RhoA/Rho kinase (show ROCK2 Antibodies) pathway and muscle contraction.
Impaired denitrosylation is associated with detrusor overactivity, which is linked with upregulated RhoA/Rho-kinase (show ROCK2 Antibodies) signalling
The in vivo function of RhoA in corpus luteum (CL) luteal cell cytoskeleton integrity, cholesterol transport, StAR expression, and progesterone synthesis, and a positive feedback on StAR expression in CL by progesterone signaling.
Reveal novel intracellular signaling mechanisms involving RhoA/STAT3 (show STAT3 Antibodies) underlying the contribution of reactive astrocyte dynamics to glial scar formation.
We show that RhoA mRNA levels were significantly higher compared with the RhoB mRNA levels in ESCs (show NR2E3 Antibodies) as well in various cancer cell lines and this difference could be accounted for by differences in the activities of the corresponding promoters.
Results strongly support the hypothesis that spinal RhoA/ROCK signaling plays a central role in the neuropathic pain. In addition, simvastatin might exert its antihyperalgesic and antiallodynic effects through the attenuation of sensitization of spinal nociceptive transmission that is modulated by mechanisms dependent on the RhoA/ROCK signaling.
Findings suggest that atorvastatin attenuates diabetes-associated renal injury by reducing reactive oxygen species (ROS (show ROS1 Antibodies)) generation, RhoA activity and normalizing Akt (show AKT1 Antibodies)/GSK3beta (show GSK3b Antibodies) signaling pathways.
findings describe a novel RhoA regulatory mechanism.
RhoA and membrane fluidity mediates the spatially polarized Src (show SRC Antibodies)/FAK (show PTK2 Antibodies) activation in response to shear stress.
the Lbc (show AKAP13 Antibodies)/alpha-catulin (show CTNNAL1 Antibodies) axis participates in 5-HT (show DDC Antibodies)-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 Antibodies)-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 Antibodies)+)](i), as well as the voltage-dependent Ca(2 (show CA2 Antibodies)+) 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.
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 Antibodies) phosphorylation, thereby activating cell proliferation and migration in bovine aortic endothelial cells.
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.
ras homolog gene family, member A
, transforming protein RhoA
, aplysia ras-related homolog A2
, Aplysia ras-related homolog 12
, oncogene RHO H12
, rho cDNA clone 12
, small GTP binding protein RhoA
, plysia ras-related homolog A2
, rho1 GTP-binding protein
, Rho A
, Ras family member A
, Rho family GTPase
, aplysia ras-related homolog A
, aplysia ras-related homolog A1
, ras homolog A1
, ras homolog A2
, ras homolog gene family, member A1
, ras homolog gene family, member A2
, RhoA GTPase