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Validated All-in-One™ qPCR Primer for RHOA(NM_001313941.2) Search again
Product ID:
HQP149855
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ARH12, ARHA, EDFAOB, RHO12, RHOH12
Gene Description:
ras homolog family member A
Target Gene Accession:
NM_001313941.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- Altogether, these results identify a mechanism by which RhoB but not RhoA antagonizes TGF-beta action through transcriptional down-regulation of AP1 in T beta R-II promoter.
- Consequences of mevalonate depletion. Differential transcriptional, translational, and post-translational up-regulation
- Expressed in myometrium
- Our findings indicate that different signaling cascades resulting in the activation of RhoA... can modulate the exocytotic process of neuroendocrine cells.
- role in sustaining integrin alphaIIbbeta3 adhesion contacts under high shear
- inhibition of protein geranylgeranylation and RhoA pathways induce apoptosis in HUVEC and that induction of p53 or other proapoptotic proteins is required for this process
- Data show that TGF-beta-induced rearrangements of the actin filament system required the activity of the Rho GTPases Cdc42 and RhoA, because ectopic expression of dominant negative mutant Cdc42 and RhoA abrogated the response.
- Structural basis for the selective activation of Rho GTPases by Dbl exchange factors.
- existence of a novel molecular mechanism by which Galpha(q) and the large family of G(q)-coupled receptors can regulate the activity of Rho and its downstream signaling pathways
- Leukotriene D4 induces association of active RhoA with phospholipase C-gamma1 in intestinal epithelial cells.
- RhoA play essential role in regulating the formation of dendritic processes by dendritic cell
- cGMP-dependent protein kinase inhibits serum-response element-dependent transcription by inhibiting rho activation and functions
- Data show that protein kinase C delta (PKC delta) is located downstream of RhoA and that active RhoA and PKCdelta are both necessary for leukotriene D(4)-induced stress-fibre formation.
- These results demonstrate that Rho family small GTPases RhoA, Rac1 and Cdc42 are novel signal transducers for SP-stimulated IL-8 expression.
- acted on by XPLN, a guanine nucleotide exchange factor
- RhoA is a novel signal transducer for bacterial lipopolysaccharide-induced Toll-like receptor 4-mediated proinflammatory cytokine synthesis in monocytes.
- These data indicate that Rho GTPases, most likely RhoA, play an important role in uterine epithelial RL95-2 cells for trophoblast binding, and suggest that RhoA may be involved in local signalling cascades during early embryo implantation in vivo.
- Results suggest a novel mechanism of RA signaling, which involves activation of TGase and transamidation of RhoA.
- a role for RhoA in mediating tumor metastasis independent of their affects on cell proliferation
- basal release of NO is necessary to maintain RhoA expression and RhoA-dependent functions in vascular smooth muscle cells
- RhoA signaling and cytoskeletal rearrangement are observed in prostate cancer cells, most likely the result of direct PAR1 and PAR2 activation by serine proteases thrombin and trypsin.
- RhoA-mediated signaling may regulate different events in SCLC and NSCLC cells, including adhesion of SCLC cells and proliferation of NSCLC cells.
- Data show that inhibition of endogenous RhoA, Rac1, and Cdc42 by their respective dominant negative mutants inhibits neurotensin-induced interleukin-8 protein production and promoter activity.
- ADP-ribosylated form activates phospholipase D1
- RhoA activation plays an integral role in tissue factor expression in endothelial cells.
- evidence that the small GTPases RhoA and Rac1, but not Cdc42, are directly associated with Tyk2 and PI3-K in an uPA/uPAR-dependent fashion and are necessary to mediate the uPA/uPAR-directed migration via the Tyk2/PI3-K signalling complex in human VSMC
- Rho activation signals interaction of IP3R with TRPC1 at the plasma membrane of endothelial cells, and triggers Ca2+ entry following store depletion and the resultant increase in endothelial permeability
- These findings show that vasodilator-stimulated phosphoprotein and diaphanous 1 function cooperatively downstream of Rho to control F-actin assembly and serum response factor activity.
- Up-regulation of this protein is associated with tumor progression in ovarian carcinoma.
- RhoA is involved in the control of the filamentous actin/monomeric actin balance through mDia, and this balance is critical for T cell responses.
- RhoGAP-Rho chimeras specifically down-regulate RhoA, RhoB and RhoC activity and demonstrated that this approach may be applied to multiple human tumor cells to reverse the growth and/or invasion phenotypes associated with a distinct subtype of Rho GTPase
- Rac1 and RhoA bind to adherens junctions and myosin light chain during formation of capillary vascular network
- The reorganization of actins into podosomes is controlled by RHOA.
- M-RIP can assemble a complex containing both RhoA and Myosin phosphatase myosin binding subunit, suggesting that M-RIP may play a role in myosin phosphatase regulation by RhoA
- analysis of the interaction between the small G proteins Rac1 and RhoA and protein kinase C-related kinase 1
- RhoA binds to the amino terminus of
- activation of Rho GTPases and coordinated rearrangement of F-actin within uterine epithelial cells in response to trophoblast binding are part of a generalized structural and functional reorganization of the cytoplasm.
- actin and RhoA are involved in inhibition of tumor cell motility by antineoplastic agents
- propose that RhoA triggers signalling pathways that, upregulating expression of a proteinase at specific membrane localizations, may confer an highly invasive phenotype to endothelial cells
- Smurf1 links the Cdc42/Rac1-PAR6 polarity complex to degradation of RhoA in lamellipodia and filopodia to prevent RhoA signaling during dynamic membrane movements
- ROCKI interacts with the switch regions of RhoA
- Activation of Rho is key mechanisms by which collagen I provokes capillary morphogenesis of microvascular endothelial cells
- rhoA and rac-1 participate in cell sensitivity to mechanical strain and lead to the modulation of the Erk pathway
- GIT1 redistribution occurs independently of Rac and requires RhoA and Rho kinase.
- Cell shape regulated the switch in lineage commitment by modulating endogenous RhoA activity. Expressing dominant-negative RhoA committed hMSCs to become adipocytes, while constitutively active RhoA caused osteogenesis
- RhoA, mDia, and ROCK have roles in cell shape-dependent control of the Skp2-p27kip1 pathway and the G1/S transition
- RhoA is another regulatory element for the completion of store-operated calcium entry-induced phosphatidylserine transmembrane redistribution in megakaryocytes
- RhoA/Rho-kinase pathway followed by tyrosine phosphorylation of FAK and paxillin leads to ATP release and actin reorganization in vascular endothelium
- Potassium chloride acts in part through stimulation of Rho and ROCK, possibly secondary to voltage-dependent Ca2+ influx
- GTPase RhoA and atypical protein kinase Czeta are required for TLR2-mediated gene transcription.
- Coordination of both RhoA and Rac1 activity contributes to bronchial epithelial wound repair mechanisms in vitro.
- RhoA activity is regulated in a cell-specific manner during cytokinesis
- Results indicate that phospholipase Cepsilon is a direct downstream effector for RhoA and that RhoA-dependent activation of PLC-epsilon depends on a unique insert within the catalytic core of the phospholipase.
- RhoA binds to leukemia-associated Rho guanine-nucleotide exchange factor
- RhoA may play a critical role in the carcinogenesis of gastric cancer
- multiple effector-binding sites in RhoA have roles in effector activation
- RhoA/Rho-kinase pathway is an important component of TGF-beta-induced effects on endothelial myosin light chain phosphorylation, cytoskeletal reorganization, and barrier integrity. (RhoA)
- DH domain makes several specific interactions with RhoA residues not conserved among other Rho family members, suggesting the molecular basis for the observed specificity
- The antagonistic roles of RhoA and Rac1 in cell motility/invasion and cytoskeletal organization in breast cancer may be due to their concerted action on NHE1 activity as a convergence point.
- The RhoA pathway signals thrombin-induced ICAM-1 expression through activation of I kappa B kinase, which promotes NF-kappa B binding to ICAM-1 promoter and phosphorylation of RelA/p65, thus mediating transcriptional activation of bound NF-kappa B.
- RhoA impedes and RhoC stimulates invasion in breast cancer.
- OxLDL has a dual effect on cell-cycle progression via regulation of p27(Kip1) expression, resulting in cellular proliferation and hypertrophy, involving activation of RhoA
- up-regulation of RhoA induced by low-oxygen conditions may play an important role in regulation of HIF-1alpha expression in trophoblast cells.
- epithelial cell motility is modulated by integrin engagment through RhoA/ROCK and PAK1
- in thrombin-stimulated endothelial cells, the unprocessed form of RhoA is rapidly geranylgeranylated to become the mature form, which then is converted into GTP-bound active RhoA
- prenylated proteins (at least RhoA, RhoB and/or RhoC) antagonize the ability of ERalpha and ERbeta to stimulate ERE-dependent transcriptional activity, potentially acting through both AF-1 and AF-2 transcriptional activities
- these results indicate that RhoA differentially modulates cancer cell death depending on the anticancer agent.
- siRNAs inhibited cell proliferation and invasion more effectively than conventional blockers of Rho cell signaling
- formation of the LPA receptor/PDZ domain-containing RhoGEF complex plays a pivotal role in LPA-induced RhoA activation
- The small GTP-binding protein RhoA is able to stimulate the phospholipid phosphatase activity of PTEN in human embryonic kidney cells and leukocytes.
- fMLP-induced activation of NF-kappaB utilizes a signaling pathway requiring activity of PKCepsilon, a signaling component downstream of RhoA in cytokine gene transcription stimulated by a chemoattractant
- RhoA has a role in ABCA1-mediated cholesterol efflux
- a pseudopodial-located RhoA/ROCK/p38/NHE1 signal module is regulated by Protein Kinase A gating and then regulates invasion in breast cancer cell lines
- Ser188 phosphorylation-mediated protection against degradation is a physiological process regulating the level of endogenous RhoA and define a novel function for RhoGDI, as an inhibitor of Rho protein degradation.
- Activation of small RhoGTPases is a key step in the mechanism of epithelial mesemchymal transdifferentiation and likely to be a contributor to tubulointerstitial fibrosis.
- study suggests that RhoA may represent a key molecule in the signalling transduction pathway of profibrotic signals in IgA nephropathy
- overexpression of the active form of the small GTPase RhoA induces the activation of Epidermal Growth Factor Receptor and promotes cell motility
- Rho signaling exerts an unexpectedly complex role in keratinocyte differentiation, which is coupled with induction of KyoT1/2, a LIM domain protein gene with a potentially important role in control of cell self renewal.
- Central spindle localization of ECT2 assists division plane positioning and the CYK-4 subunit of centralspindlin acts upstream of RhoA to promote furrow assembly.
- Cdk1 inactivation is sufficient to activate a signaling pathway leading to cytokinesis, which emanates from mitotic spindles and is regulated by ECT2, MgcRacGAP, and RhoA
- phosphorylation of ECT2 leads to accumulation of RHOA
- The results suggest that oncogenic K-Ras enhances the malignant phenotype and identify the mitogen-activated protein kinase p38 as a target to inhibit oncogenic K-Ras-induced pancreatic tumor cell migration.
- FAK-induced down-modulation of RhoA activity via p190RhoGAP is a crucial step in signaling endothelial barrier restoration after increased endothelial permeability
- Data show that RhoA accumulates at the equatorial cortex before furrow initiation and continues to concentrate at the cleavage furrow during cytokinesis, and that centralspindlin and ECT2 are required for this localization and furrowing.
- HEF1 associates with the RhoA-GTP exchange factor ECT2, an orthologue of the Drosophila cytokinetic regulator Pebble, providing a direct means for HEF1 control of RhoA.
- Lysoophosphatidic acid stimulates RhoA and increased PC-3 prostate cancer cell invasion activity through an NF-kappaB-dependent pathway.
- findings show that the vaccinia F11L protein interacts directly with RhoA, inhibiting its signaling by blocking the interaction with its downstream effectors Rho-associated kinase (ROCK) and mDia
- Data show that the HR1 region is necessary but not sufficient in eliciting a full activation of PRK1 upon binding of RhoA, and that activation is controlled by the very C-terminus of PRK1.
- Rnd2 regulates neurite outgrowth by functioning as the RhoA activator through Pragmin, in contrast to Rnd1 and Rnd3 inhibiting RhoA signaling
- REVIEW: cytoskeleton-regulated RhoA signaling cooperates with PKC activation constitutes a cellular context to determine the cell fate in response to phorbol ester stimulation
- CB2 might play a role in regulating excessive inflammatory response by controlling RhoA activation, thereby suppressing neutrophil migration
- F-actin constrains cell polarity by locally reducing activation of RhoA, thereby reducing its active form at the front. Mutual incompatibility of frontness and backness is responsible for self-organization of neutrophil polarity.
- Escherichia coli producing cytotoxic necrotizing factor and transforming growth factor-beta trigger activated RhoA ubiquitylation through Smurf1 ubiquitin-ligase.
- Synaptopodin, an actin-associated protein, as a novel regulator of RhoA signalling and cell migration in kidney podocytes.
- cGMP-dependent protein kinase expression is regulated by Rho and Kruppel-like transcription factor-4
- PTP1B mediates of RhoA-dependent phosphorylation of p130Cas.
- Our data indicate that TGF-beta1 induces endothelial barrier dysfunction involving Smad2-dependent p38 activation, resulting in RhoA activation by possible transcriptional regulation.
- Both neuropeptides that activate G-protein-coupled receptors and growth factors that activate receptor tyrosine kinases require RhoA to induce prostate cancer cell migration.
- These findings indicate for the first time that activation of geranylgeranylated proteins including RhoA and Rac1 is involved in type III GBS invasion of HBMEC and RhoA is upstream of Rac1 in GBS invasion of HBMEC.
- In human lung fibroblasts, bradykinin modulates the action of AngII through the small G protein RhoA, but in a Galphai/Galphaq-independent manner.
- the role of RhoA GTPase in protein kinase D activation depends on the cellular localization of protein kinase D
- cyclin D1 expression is deregulated in idiopathic pulmonary fibrosis through a RhoA dependent mechanism that influences lung fibroblast proliferation
- PIP3 and Cdc42 maintain stable polarity with a single front and a single back not only by strengthening pseudopods but also, at longer range, by promoting RhoA-dependent actomyosin contraction at the trailing edge.
- These results demonstrate that MAGI-3 interacts directly with LPA(2) and regulates the ability of LPA(2) to activate Erk and RhoA.
- our study demonstrates increased expression of RhoA in high-grade astrocytomas
- study investigated the role of RhoA and Rho-kinase in endothelial eNOS protein expression under hypoxic conditions
- Because of its efficacy and the absence of toxicity, it is suggested that this strategy of anti-RhoA siRNA holds significant promise for the treatment of aggressive cancers.
- RhoA and RhoC are downstream of PKC epsilon & critical for PKC-epsilon-mediated cell invasion & motility. PKC epsilon coordinately regulates RhoA & RhoC activation, possibly through direct post-translational phosphorylation.
- findings suggest a new, 2-faced role for RhoA as a checkpoint in innate immunity
- ARAP2 is an Arf6GAP that functions downstream of RhoA to regulate focal adhesion dynamics.
- gene copy multiplication and demethylation of the RHOA promoter region can contribute to transcription activation of this gene in epithelial tumors
- These findings support an essential role for p0071 in spatially regulating restricted Rho signalling during cytokinesis.
- In this study, we provide evidence that PV-immunoglobulin G (IgG) and PF-IgG induce skin blistering by interference with Rho A signaling.
- Silencing of RhoA expression with siRNA increased the levels of E-cadherin and alpha-catenin in colon cancer cell ines.
- These results suggest that Smurf1 is a pivotal regulator of tumor cell movement through its regulation of RhoA signaling.
- Galphaq activation of TRPC6 signals the activation of PKCalpha, and thereby induces RhoA activity and endothelial cell contraction
- RhoA signaling has a role in lung cancer
- The RhoA gene, rs2878298, showed highly significant genotypic association with both smoking initiation (SI) and nicotine dependence (ND). In the allelic analyses, rs2878298 was only significant for SI.
- RGS3L functions as a molecular switch, redirecting Gi-coupled receptors via Gbetagamma-dimers and PI3K from Rac1 to RhoA activation.
- Increases in GTP-bound RHOA and DIAPH1 expression may contribute to the increase in uterine activity in idiopathic preterm labor.
- Maspin control mammary tumor migration through inhibiting Rac1 and Cdc42, but not RhoA GTPase.
- These data suggest that p53 suppresses cancer progression to malignancy by modulating the quality of Ras signaling.
- NHERF1 overexpression enhances the invasive phenotype in breast cancer cells, both alone and in synergy with exposure to the tumor microenvironment, via the coordination of PKA-gated RhoA/p38 signaling.
- Polo-like kinase 1 has a role in positioning RhoA and triggering cytokinesis in human cells
- Plk1 and RhoA function to enhance Rock2 kinase activity in vitro and within cells, and implicate Plk1 as a regulator of multiple pathways that synergistically converge to regulate actomyosin ring contraction during cleavage furrow ingression.
- These results identify a GEF-H1-dependent mechanism to modulate localized RhoA activation during cytokinesis under the control of mitotic kinases.
- These results suggest that the TTC3-RhoA-CIT-K pathway could be a crucial determinant of in vivo neuronal development, whose hyperactivity may result in detrimental effects on the normal differentiation program.
- Activation of PAR1-induced dynamic cytoskeletal reorganization and reduced PC-3 binding to collagen I, collagen IV, and laminin (P < 0.01) but not fibronectin.
- analysis of a novel cross-talk exerted from the LPA/Galpha(13)/p115RhoGEF/RhoA pathway to the beta(2)-adrenergic receptor/Galpha(s)/adenylyl cyclase pathway
- NFAT-dependent gene expression was modulated by the RhoA signaling pathway in T-lymphocytes.
- Data suggest that lipid rafts play critical roles in KSHV infection and gene expression, probably due to their roles in modulating KSHV-induced PI3-K, RhoA-GTPase, and Dia-2 molecules essential for postbinding and entry stages of infection.
- Results of this study suggest that the Rho-family GTPases are required for efficient invasion of HeLa cells by GBS.
- Ang-1 phosphorylates Tie-2 and its downstream effector phosphatidylinositol 3-kinase. This induces activation of one endogenous GTPase, Rac1, and inhibition of another, RhoA
- findings suggest that the RhoA is related to malignant transformation and progression of colorectal cancer and the activation of RhoA is associated with lymph node metastasis.
- Co-immunoprecipitation reveals that RhoA and polo-like kinase 1 physically interact and that their interaction appears to be enhanced during mitosis.
- the crucial role of the phosphorylation of the C terminus of GDI-1 at S96 in selectively activating RhoA
- Inhibitory role of RHOA on senescence-like growth arrest by a mechanism involving modulation of phosphatase activity is reported.
- These results suggest the existence of a feedback loop between cytoskeletal tension, adhesion maturation, and ROCK signaling that likely contributes to numerous mechanochemical processes.
- FGFR-mediated phosphorylation of ephexin1 enhances the guanine nucleotide exchange activity toward RhoA without affecting the activity to Rac1 or Cdc42.
- Sphingosine 1-phosphate inhibited monocyte-endothelial interactions by inhibiting RhoA activity which may explain its anti-atherogenic effects
- plexin-B1 promotes endothelial cell motility through RhoA and ROK by regulating the integrin-dependent signaling networks that result in the activation of PI3K and Akt
- High expression of RHOA is associated with esophageal squamous cell carcinoma
- Expression level of RhoA is correlated with tumor progression and metastasis in hepatocellular carcinoma.
- BMP signaling modulates VSMC phenotype via cross-talk with the RhoA/MRTFs pathway, and may contribute to the development of the pathological characteristics observed in patients with PAH and other obliterative vascular diseases.
- tethering of RhoA to the membrane by GGpp is determinant for T cell migration
- OLIG2 suppresses the motile phenotype of glioblastoma cells by activating RhoA.
- These results indicate that START-GAP3/DLC3 has characteristics similar to other START-GAPs and the START-GAP family seems to share common characteristics.
- The vaccinia virus-induced increases in peripheral microtubule dynamics require F11L-mediated inhibition of signaling via the GTPase RhoA and its effector, mDia.
- cortical movements and the subsequent release of vaccinia virus particles, which are both actin dependent, require F11L-mediated inhibition of RhoA-mDia signaling.
- These results suggest induction of SRF-mediated transcription by alpha(E)-catenin either downstream of RhoA or via a parallel pathway.
- Rho kinase and ERK1/2 play more important roles than RhoA in PGE(2)-mediated migration stimulation of first-trimester trophoblasts.
- These results suggest that S1P(2) receptors/G(12/13)-proteins/Rho signaling pathways mediate S1P-induced inhibition of glioma cell migration.
- the crystal structure of the Galphaq-p63RhoGEF-RhoA complex, detailing the interactions of Galphaq with the Dbl and pleckstrin homology (DH and PH) domains of p63RhoGEF was determined
- TBXA2R are expressed in prostate cancer and activation of TBXA2R regulates prostate cancer cell motility and cytoskeleton reorganization through activation of RhoA.
- reveal PECAM-1 signaling and interactions with the cytoskeleton, which are required for CAM-endocytosis, and may provide safe intra-endothelial drug delivery by anti-PECAM/nanocarriers
- data suggest that EPHA2 promotes tumor malignancy through a mechanism involving RhoA-dependent destabilization of adherens junctions
- TGFbeta1 stimulates CCN2 expression in human gingival fibroblasts through a RhoA-independent, Rac1/Cdc42-dependent mechanism
- These studies reveal a critical role for a GEF-H1/RhoA/ROCK/MLC signaling pathway in mediating nocodazole-induced cell contractility.
- Particular chemokine signals activate, within subseconds, the RhoA 23/40 domain to induce lymphocyte function-associated antigen-1 (LFA-1) extension and thereby trigger LFA-1-mediated lymphocyte arrest on ICAM-1.
- in SGC-7901 gastric cancer cells RhoA was found to be localized within the membrane, the cytosol, and the nucleus
- Data suggest that TGF-beta1 induces human retinal pigment epithelial cells to undergo cytoskeletal actin rearrangement via RhoA GTPase-dependent pathways that modulate LIM kinase and cofilin activity.
- TGFBR1*6A may contribute to cancer progression through RhoA activation in a TGF-beta signaling-independent manner
- The purpose of this study was to characterize the significance of Rho processes in the cellular cytoskeleton.
- These data indicate a novel role for RhoA as a negative regulator of HIF-1alpha.
- Human ARHGAP6 protein possessing GTPase stimulating activity for RhoA on the catalytic properties of PLC-delta1, was studied.
- findings show the BNIP2 & BCH domain of BNIPXL interacts with specific conformers of RhoA & mediates association with catalytic DH-PH domains of Lbc, a RhoA-specific guanine nucleotide exchange factor; BNIPXL inhibits Lbc-induced oncogenic transformation
- Data suggest that Kank negatively regulates the formation of actin stress fibers and cell migration through the inhibition of RhoA activity, which is controlled by binding of Kank to 14-3-3 in PI3K-Akt signaling.
- RhoA/Rho-associated kinase signaling plays positive and negative roles in myogenic differentiation, mediated by MRTF-A/Smad-dependent transcription of the Id3 gene in a differentiation stage-specific manner
- RhoA protein expression correlated with overall survival of patients with pancreatic ductal adenocarcinoma..
- The effect of OGP(10-14) on differentiation of a cancer megakaryoblast cell line and its involvement on RhoA and Src family kinases signaling pathway, was evaluated.
- RhoA mediated cell survival in cells exposed to DNA damaging agents is modulated by Net1
- in basal conditions, RhoGDIalpha is rate-limiting and the suppression of RhoA makes it available to stabilize RhoB
- The exocyst subunits Sec3 and Sec8 interact with the polarity protein IQGAP1 and that this interaction is triggered by active Cdc42 and RhoA, which are essential for matrix degradation.
- activation of the RhoA GTPase was defective in VHL(-) cells, and this was possibly mediated by an increased activation of its inhibitor, p190RhoGAP.
- The association of lymphocyte RhoA protein expression with classical clinico-pathological parameters closely corresponded with that observed for RhoA protein expression in the tumor biopsies.
- WNK2 controls a RhoA-mediated cross-talk mechanism that regulates the efficiency with which MEK1 can activate ERK1/2 upon growth factor stimulation.
- Ca(2+) sensitization mediated by the RhoA-kinase pathway has an important role in contraction of human esophageal body (EB) and lower esophageal sphincter (LES) muscles.
- decreased DLC2 expression in hepatocellular carcinoma correlates with cell differentiation and overexpression of RhoA associated with poor prognosis
- Netrin 1, through its receptor DCC, inhibits RhoA in embryonic spinal commissural neurons.
- ABL2/ARG is a novel mediator of SEMA3F-induced RhoA inactivation and collapsing activity.
- Thrombin receptor and RhoA mediate cell proliferation through integrins and cysteine-rich protein 61.
- Interleukin-13 augments bronchial smooth muscle contractility with an up-regulation of RhoA protein.
- Data suggest that RhoA and B small GTPases, along with ROCK, are major membrane androgen receptor effectors controlling actin reorganization and apoptosis in prostate cancer cells.
- Protein kinase C-related kinase and ROCK are required for thrombin-induced endothelial cell permeability downstream from Galpha12/13 and Galpha11/q
- Staphylococcal enterotoxin B-treated renal proximal tubule epithelial cells show down regulation of Rnd3 and mRNA for RhoA was shown to increase.
- RhoA mRNA expression is significantly lower in cancerous as compared to normal kidney tissue. RhoA protein expression is significantly higher in normal than in cancerous tissues.
- a link between RhoA, JNK, c-Jun, and MMP2 activity that is functionally involved in the reduction in osteosarcoma cell invasion by the statin. This suggests a novel strategy targeting RhoA-JNK-c-Jun signaling to reduce osteosarcoma cell tumorigenesis.
- Treatment with lysophosphatidylinositol induces marked GPR55 internalization and stimulates a sustained, oscillatory calcium release pathway, which is dependent on Galpha13 and requires RhoA activation.
- p27 promotes cell migration in metastatic HCC cells through the regulation of RhoA activity.
- the directional migration of capillaries in the embryo is governed by the Amot:Patj/Mupp1:Syx signaling that controls local GTPase activity
- the importance of NET1 as a driver of tumour cell invasion, an activity mediated by RhoA activation and cytoskeletal reorganisation.
- IMC-C225 cross-links integrins with EGFR, leading to Vav2-dependent activation of RhoA
- the last seven amino acid residues at the C-terminus of PRK2 are not required for the activation of the kinase by RhoA in vitro, however, the extreme C-terminal segment is critical for the full activation of PRK2 by RhoA in cells
- RhoA and its downstream molecule ROCK may mediate the substrate rigidity-regulated Ca(2+) oscillation, which determines the physiological functions of human mesenchymal stem cells.
- MLK3 functions in a regulated way to limit levels of the activated GTPase Rho by binding to the Rho activator, p63RhoGEF/GEFT, which, in turn, prevents its activation by Galphaq.
- G(alpha)(13)-dependent downstream effects on RhoA activation and invasion tightly depend on cell type-specific GAP activities and that G(alpha)(13)-p190RhoGAP signaling might represent a potential target for intervention in melanoma metastasis.
- RhoA pathway is implicated in suppression of MM migration and invasion
- Graf residues important for the structural integrity are critical for binding RhoA and for the catalytic activity of GAP, but GTPase selectivity appears to be modulated by a more subtle interplay involving residues on the periphery of the main interface.
- EB1 is controlled by c-Myc, RhoA, and CDC42, which have all been linked to hepatocellular carcinoma (HCC) malignancy.
- Guanosine Triphosphate binding protein, RhoA is activated downstream the Proton-Translocating ATPases /P2Y13 protein signalling payway.
- HPV16 E7-dependent transformation activates NHE1 through a PKA-RhoA-induced inhibition of p38alpha.
- Memo-RhoA-mDia1 signaling coordinates the organization of the lamellipodial actin network, adhesion site formation, and microtubule outgrowth within the cell leading edge to sustain cell motility.
- SifA, SKIP, SseJ, and RhoA family GTPases cooperatively promote host membrane tubulation.
- ARHGAP5 (the gene encoding p190-B RhoGAP) is a probable target for the amplification at 14q12, and p190-B RhoGAP promotes cells spreading and migration by negatively regulating RhoA activity in Huh-7 hepatocellular carcinoma cells
- the action of 1,25(OH)(2)D(3) on colon carcinoma cells depends on the dual action of VDR as a transcription factor and a nongenomic activator of RhoA-ROCK and p38MAPK-MSK1.
- Overexpression of RHOA enhances peritoneal dissemination: RHOA suppression with Lovastatin may be useful for ovarian cancer.
- analysis of the the antiparallel coiled coil motif from PKN complexed with RhoA
- Ectopic expression of wild-type (WT) RhoA as well as a constitutively active RhoA mutant (G14V) in two independent primary human mammary gland epithelial cells strains led to their immortalization and preneoplastic transformation.