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Rho GTPase activating protein 5 negatively regulates RHO GTPases, a family which may mediate cytoskeleton changes by stimulating the hydrolysis of bound GTP. Additionally we are shipping ARHGAP5 Antibodies (17) and and many more products for this protein.
Kazrin (show KAZ ELISA Kits) interacts with ARVCF (show ARVCF ELISA Kits)-catenin, spectrin and p190B RhoGAP (show ARHGAP1 ELISA Kits), and modulates RhoA (show RHOA ELISA Kits) activity.
This newly identified miR (show MLXIP ELISA Kits)-744/ARHGAP5 pathway provides further insight into the progression and metastasis of NPC (show NPC1 ELISA Kits) and indicates potential novel therapeutic targets for NPC (show NPC1 ELISA Kits).
Ectopic expression of p190B suppressed the miR (show MLXIP ELISA Kits)-494-induced EGFR (show EGFR ELISA Kits) upregulation.
The expression level of miR (show MLXIP ELISA Kits)-486-5p was inversely correlated with that of ARHGAP5.
RhoA (show RHOA ELISA Kits) is down-regulated at cell-cell contacts via p190RhoGAP (show GRLF1 ELISA Kits)-B in response to tensional homeostasis.
Data indicate a role for p120-catenin (amino acids 820-843) domain in the p120-catenin.p190RhoGAP signaling complex assembly and membrane targeting.
A cell cycle-regulated reduction in endogenous p190 (show CNTNAP1 ELISA Kits) levels is linked to completion of cytokinesis and generation of viable cell progeny.
precise control of p190-B Rho GTPase-activating protein activity is critical for normal branching morphogenesis during mammary gland development
ARHGAP5 (the gene encoding p190-B RhoGAP (show ARHGAP1 ELISA Kits)) is a probable target for the amplification at 14q12, and p190-B RhoGAP (show ARHGAP1 ELISA Kits) promotes cells spreading and migration by negatively regulating RhoA (show RHOA ELISA Kits) activity in Huh-7 hepatocellular carcinoma cells
Results link Cdk5 (show CDK5 ELISA Kits) to Rho-ROCK signaling via Src (show SRC ELISA Kits) and p190RhoGAP (show GRLF1 ELISA Kits) and implicate Cdk5 (show CDK5 ELISA Kits) in the regulation of cell contraction, attachment, and migration.
Loss of p190-B expression is associated with defective hematopoiesis.
Rac1 activity and oxidative stress are elevated in tumors expressing exogenous p190B suggesting that p190B may promote tumorigenesis through a Rac1/ROS (show ROS1 ELISA Kits) dependent mechanism.
p190B haploinsufficiency in the epithelium inhibits MMTV-Neu tumor initiation. p190B deficiency in the vasculature is responsible, in part, for the inhibition of MMTV-Neu tumor progression.
Mice lacking the Rho-inhibitory protein, p190-B RhoGAP (show ARHGAP1 ELISA Kits), are 30% reduced in size and exhibit developmental defects strikingly similar to those seen in mice lacking the CREB (show CREB1 ELISA Kits) transcription factor.
Results suggest that p190-B regulates ductal morphogenesis, at least in part, by modulating the IGF signaling axis
IGF signaling through p190-B and IRS (show IARS ELISA Kits) proteins is critical for mammary bud formation and ensuing epithelial-mesenchymal interactions necessary to sustain mammary bud morphogenesis
Loss of the Rho GTPase activating protein p190-B enhances hematopoietic stem cell engraftment potential.
Rho GTPase activating protein 5 negatively regulates RHO GTPases, a family which may mediate cytoskeleton changes by stimulating the hydrolysis of bound GTP. Two transcript variants encoding different isoforms have been found for this gene.
Rho GTPase activating protein 5
, chimerin (chimaerin) 1-like
, rho GTPase-activating protein 5-like
, growth factor independent 2
, p100 RasGAP-associated p105 protein
, p105 RhoGAP
, rho GTPase-activating protein 5
, rho-type GTPase-activating protein 5