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anti-Human RHOA Antibodies:
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Human Polyclonal RHOA Primary Antibody for IHC, WB - ABIN6714711
Zhang, Bian, Li, Liu, Sun, Li, Zhang, Ji: ERK-MAPK signaling opposes rho-kinase to reduce cardiomyocyte apoptosis in heart ischemic preconditioning. in Molecular medicine (Cambridge, Mass.) 2010
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Human Monoclonal RHOA Primary Antibody for IF, IHC (p) - ABIN559931
Bu, Erlander, Hitz, Tillakaratne, Kaufman, Wagner-McPherson, Evans, Tobin: Two human glutamate decarboxylases, 65-kDa GAD and 67-kDa GAD, are each encoded by a single gene. in Proceedings of the National Academy of Sciences of the United States of America 1992
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Human Polyclonal RHOA Primary Antibody for ELISA, WB - ABIN548452
Sawada, Itoh, Yamashita, Doi, Inoue, Masatsugu, Fukunaga, Sakaguchi, Sone, Yamahara, Yurugi, Nakao: cGMP-dependent protein kinase phosphorylates and inactivates RhoA. in Biochemical and biophysical research communications 2001
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Human Polyclonal RHOA Primary Antibody for IF (p), IHC (p) - ABIN758242
Zhang, He, Lu, Bian, Yang, Fu, Wu, Li: HSF1 Relieves Amyloid-?-Induced Cardiomyocytes Apoptosis. in Cell biochemistry and biophysics 2015
Human Polyclonal RHOA Primary Antibody for FACS, IF (cc) - ABIN738846
Li, Sun, Yang, Hu, Jiang: Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway. in Chinese journal of integrative medicine 2014
Expression of the RHOA, RAC1 and CXCR4 proteins and their interactions play a role as risk factors for infiltration to the nipple areola complex in operable breast carcinoma.
MiR-144 inhibited tumor growth and metastasis in OS via dual-suppressing of RhoA and ROCK1.
Expression of constitutively active and dominant-negative isoforms of RHOA revealed that it acts downstream of VANGL2.
RhoA plays a critical role in diabetic nephropathy.RhoA protein expression is markedly decreased in the glomerular podocytes of patients with diabetic nephropathy.
Cobalt (II) ions and nanoparticles induce macrophage retention by ROS-mediated down-regulation of RhoA expression.
Data provide evidence for a pathway in IPF where fibroblasts down-regulate Rnd3 levels and p190 activity to enhance RhoA activity and drive the fibrotic phenotype.
Our findings revealed the critical role of CXCR4 in promoting progression of inflammatory colorectal cancer through recruiting immunocytes and enhancing cytoskeletal remodeling by lncRNA XIST/ miR-133a-3p/ RhoA signaling. These results provide novel potential therapeutic targets for hindering CXCL12/CXCR4-induced CRC progression.
SmgGDS-607 completely inhibits RhoA prenylation catalyzed by protein geranylgeranyltransferase I (GGTase-I) in an in vitro radiolabel incorporation assay. SmgGDS-607 inhibits prenylation by binding to and blocking access to the C-terminal tail of the small GTPase (substrate sequestration mechanism) rather than via inhibition of the prenyltransferase activity.
through profilin-1 binding, CLIC4 functions in a RhoA-mDia2-regulated signaling network to integrate cortical actin assembly and membrane protrusion
Mechanical cues control mutant p53 stability through a mevalonate-RhoA axis.
The S-nitrosothiols regulate myosin light chain phosphorylation by inhibiting RhoA/Rho-kinase signaling through modification of RhoA cysteine residues at 16 and 20 in its GTP-binding domain, which might be an important therapeutic target for diseases with imbalanced vascular resistance.
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.
RhoA plays a critical role in diabetic nephropathy probably by mediating the podocyte apoptosis through YAP.
Individual tumors were assessed for proliferation, apoptosis, angiogenesis, RhoA activation, and activation of PyMT-dependent signaling pathways
Study showed that flavonoids extracted from leaves of Diospyros kaki regulates RhoA activity to rescue synapse loss and reverse memory impairment in Alzheimer Disease mouse model.
Nfix is regulated through the RhoA/ROCK axis, which maintains embryonic myogenesis.
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.
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