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anti-Human RHOA Anticorps:
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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 (Montrer CASZ1 Anticorps)/Egfl7 (Montrer EGFL7 Anticorps)/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 (Montrer KAZ Anticorps) interacts with ARVCF (Montrer ARVCF Anticorps)-catenin, spectrin and p190B (Montrer ARHGAP5 Anticorps) RhoGAP (Montrer ARHGAP1 Anticorps), and modulates RhoA activity.
Morphogenesis of the primitive gut tube is generated by Rho/ROCK/myosin II-mediated endoderm rearrangements.
TET2 (Montrer TET2 Anticorps) and RhoA mutations cooperatively disrupt T cell homeostasis
Genetic variant in RhoA gene is associated with progression of prostate cancer.
Downregulation of Cul3 (Montrer CUL3 Anticorps) led to a marked increase in RhoA protein expression after 6 days of adipocytes differentiation, suggesting that Cul3 (Montrer CUL3 Anticorps) 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 (Montrer GNA13 Anticorps)) and rhoA GTP-binding protein (RhoA) in Burkitt's lymphoma and diffuse large B-cell lymphoma (DLBCL).
RhoA/ROCK and Raf-1 (Montrer RAF1 Anticorps)/CK2 (Montrer CSNK2A1 Anticorps) pathway are responsible for TNF-alpha (Montrer TNF Anticorps)-mediated endothelial cytotoxicity via regulation of the vimentin (Montrer VIM Anticorps) cytoskeleton.
Rac (Montrer AKT1 Anticorps) 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 (Montrer GUCA2A Anticorps)-1,7-diaminoheptane, a DHPS (Montrer DHPS Anticorps) inhibitor, resulted in a significant decrease in tumor formation in vivo. In patients with esophageal squamous cell carcinoma (ESCC), overexpression of DHPS (Montrer DHPS Anticorps) in ESCC tumors was significantly associated with worse recurrence-free survival, and correlated with distant metastasis.
Besides controlling cyclin (Montrer PCNA Anticorps)/CDK (Montrer CDK4 Anticorps) kinase activity, p27 (Montrer PAK2 Anticorps) also regulates cytoskeletal dynamics, cell motility and cell invasion. Following processing by caspases, p27 (Montrer PAK2 Anticorps) fails to bind to RhoA and to inhibit its activation, and thereby abolishes the ability of p27 (Montrer PAK2 Anticorps) 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 (Montrer TNF Anticorps) stimulates Rac (Montrer AKT1 Anticorps), ADAM17/TACE (Montrer ADAM17 Anticorps), and RhoA through the guanine nucleotide exchange factor (Montrer ARHGEF12 Anticorps) (GEF)-H1 (Montrer ARHGEF2 Anticorps).
Contractile pulmonary arterial myocytes exhibit marked Rho-dependent actin polymerization in hypoxia, with increased active RhoA and LIMK (Montrer LIMK1 Anticorps) phosphorylation.
Results suggest that Rac1 and RhoA are regulated by TGFbeta1 (Montrer TGFB1 Anticorps) 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 (Montrer ROCK1 Anticorps) inhibitor Y-27632 showed a stronger inhibitory effect in detrusor with intact urothelium.
Thrombin (Montrer F2 Anticorps) stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1 (Montrer F2R Anticorps), RhoA, and myocardin (Montrer MYOCD Anticorps).
Rho attenuates the interaction between Amot (Montrer AMOT Anticorps) and Nf2 (Montrer NF2 Anticorps) by binding to the coiled-coil domain of Amot (Montrer AMOT Anticorps).
we uncovered cell state plasticity and adhesion dynamics regulated by Ror2 (Montrer ROR2 Anticorps), which influenced Ras Homology Family Member A (Montrer CXCL14 Anticorps) (RhoA) and Rho-Associated Coiled-Coil Kinase 1 (ROCK1 (Montrer ROCK1 Anticorps)) activity downstream of Dishevelled-2 (Dvl2 (Montrer DVL2 Anticorps)).
Active Rho-kinase (Montrer ROCK2 Anticorps) diffuses to growing other immature neurites and inhibits their outgrowth to ensure single axon formation.
Data indicate that oxidative stress in diabetes causes a decrease in miR (Montrer MLXIP Anticorps)-133a expression leading to an increase in RhoA/Rho kinase (Montrer ROCK2 Anticorps) pathway and muscle contraction.
Impaired denitrosylation is associated with detrusor overactivity, which is linked with upregulated RhoA/Rho-kinase (Montrer ROCK2 Anticorps) 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 (Montrer STAT3 Anticorps) 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 (Montrer NR2E3 Anticorps) as well in various cancer cell lines and this difference could be accounted for by differences in the activities of the corresponding promoters.
RhoA and membrane fluidity mediates the spatially polarized Src (Montrer SRC Anticorps)/FAK (Montrer PTK2 Anticorps) activation in response to shear stress.
the Lbc (Montrer AKAP13 Anticorps)/alpha-catulin (Montrer CTNNAL1 Anticorps) axis participates in 5-HT (Montrer DDC Anticorps)-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 (Montrer PTK2 Anticorps)-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 (Montrer CA2 Anticorps)+)](i), as well as the voltage-dependent Ca(2 (Montrer CA2 Anticorps)+) 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 (Montrer PTK2 Anticorps) 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