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anti-Human GRLF1 Antibodies:
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Human Polyclonal GRLF1 Primary Antibody for IHC (p) - ABIN5579387
Li, Li, Zhou, Wang, Wang, Zhao, Cui, Ren, Dong, Chen: Abnormal expression of p190RhoGAP in colorectal cancer patients with poor survival. in American journal of translational research 2016
High ARHGAP35 expression is associated with lung adenocarcinoma.
In the Title.
report association of APOE and TOMM40 with behavioural variant frontotemporal dementia, and ARHGAP35 and SERPINA1 with progressive non-fluent aphasia.
interaction involves the first FF motif of p190A and the winged helix/PCI domain of eIF3A, is enhanced by serum stimulation and reduced by phosphatase treatment
these data demonstrate that a complex of p190RhoGAP-A and anillin modulates RhoA-GTP levels in the cytokinetic furrow to ensure progression of cytokinesis.
These results place Blk upstream of the p190RhoGAP-RhoA pathway in Galpha13-activated cells, overall representing an opposing signaling module during CXCL12-triggered invasion.
ARHGAP35 rs1052667 polymorphism was an independent prognostic factor influencing the survival of osteosarcoma.
GRF-1 expression may modify osteosarcoma prognosis and may be a potential tumor therapeutic target.
A ubiquitous binding partner of p190RhoGAP, p120RasGAP (RasGAP), is expressed in much lower levels in DKO4 cells compared to DLD1, and this expression is regulated by KRAS.
Overexpression of p190 mRNA associated with lung adenocarcinoma.
These data suggest that the interaction of human papillomavirus E7 with p190 dysregulates this GTPase activating protein and alters the actin cytoskeleton.
RhoA is down-regulated at cell-cell contacts via p190RhoGAP-B in response to tensional homeostasis.
These results suggest that folic acid might inhibit endothelial cell migration through inhibiting the RhoA activity mediated by activating the FR/cSrc/p190RhoGAP-signaling pathway.
role of the N-terminal region in signaling; Rnd1 and Rnd3 have a KERRA (Lys-Glu-Arg-Arg-Ala) sequence of amino acids in their N-terminus, which functions as the lipid raft-targeting determinant; the sequence mediates lipid raft targeting of p190 RhoGAP correlated with its activation
A neutrophil- and ss2 integrin-dependent transgenic model of the effector phase of autoimmune arthritis proceeds normally in p190RhoGAP-deficient bone marrow.
in addition to activation of RhoGEF(s), reduction of RhoGAP (p190) is a critical mechanism by which increased RhoGTP levels are achieved in late mitosis, thereby ensuring proper cell division.
Cdh1 formed a physical complex with p190 and stimulated the efficient ubiquitination of p190, both in in vitro and in vivo.
p190 transiently associates with plexins, and its RhoGAP activity is increased in response to semaphorin stimulation. We conclude that p190-RhoGAP is crucially involved in semaphorin signalling to the actin cytoskeleton, via interaction with plexins.
FAK-induced down-modulation of RhoA activity via p190RhoGAP is a crucial step in signaling endothelial barrier restoration after increased endothelial permeability
By linking Rac1 activation and RhoA inhibition, p190 RhoGAP is critical to the protective effects of Ang-1 against endotoxin.
p190A acts as a modulator of Rho GTPases in a localized area around the cilia to permit the dynamic actin rearrangement required for cilia elongation.
The cellular RacGAP activity of p190RhoGAP requires an intact polybasic region adjacent to the GAP domain whereas the RhoGAP activity is inhibited by the same domain.
study demonstrates that the epidermal growth factor receptor (EGFR) cooperates with beta3 integrin to regulate p190RhoGAP activity in mammary gland epithelial cells
p190RhoGAP links integrins and caveolin-1/caveolae to RhoA in a mechanotransduction cascade that participates in endothelial adaptation to flow.
In a novel knockout mouse strain p190RhoGAP does not play a major, indispensable role in integrin signaling of neutrophils.
identified the serum-responsive transcriptional regulator TFII-I as a specific interactor with the p190 RhoGAP FF domains
Rac activation links diverse signaling systems to adherens junction assembly by controlling transient p190RhoGAP interactions with p120 and localized inhibition of Rho.
These data strongly suggest that Arg inhibits cell migration by restricting actomyosin contractility and regulating its coupling to the substrate through focal adhesions.
Signaling through p190RhoGAP acts late during synaptic refinement to promote dendritic spine maturation and synapse/dendrite stability by attenuating synaptic Rho activity.
p190RhoGAP as the convergence point for adhesive signals mediated by alpha(5)beta(1) integrin and syndecan-4.
Data show that fibroblast, endothelial and carcinoma polarity during cell migration requires FAK and is associated with a complex between FAK, p120RasGAP and p190RhoGAP (p190A), leading to p190A tyrosine phosphorylation.
The human glucocorticoid receptor DNA binding factor, which associates with the promoter region of the glucocorticoid receptor gene (hGR gene), is a repressor of glucocorticoid receptor transcription. The amino acid sequence deduced from the cDNA sequences show the presence of three sequence motifs characteristic of a zinc finger and one motif suggestive of a leucine zipper in which 1 cysteine is found instead of all leucines. The GRLF1 enhances the homologous down-regulation of wild-type hGR gene expression. Biochemical analysis suggests that GRLF1 interaction is sequence specific and that transcriptional efficacy of GRLF1 is regulated through its interaction with specific sequence motif. The level of expression is regulated by glucocorticoids.
glucocorticoid receptor DNA binding factor 1
, glucocorticoid receptor DNA-binding factor 1
, glucocorticoid receptor repression factor 1
, rho GAP p190A
, rho GTPase-activating protein 35
, P190 RhoGAP
, GAP-associated protein p190
, Rho GTPase activating protein 35 L homeolog
, rho GTPase activating protein 35 L homeolog