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Novel mercaptoacetamide-based class II histone deacetylase (show HDAC1 Proteins) inhibitor HDACIW2 treatment regulated the levels of RasGRF1 (show RASGRF1 Proteins) and p-ERK (show EPHB2 Proteins), and that W2 requires RasGRF1 (show RASGRF1 Proteins) and ERK (show EPHB2 Proteins) signaling to alter dendritic spine formation, suggesting that W2 regulates dendritic spine formation via a RasGRF1 (show RASGRF1 Proteins)/ERK (show EPHB2 Proteins)-dependent signaling pathway
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.
Data (including data from studies in knockout mice) suggest mechanisms involving RasGRF1 (show RASGRF1 Proteins) exist to regulate hypothalamic-pituitary-adrenal axis in early-adolescent females; such mechanisms appear absent in younger/older female or adolescent male mice.
VLDLR (show VLDLR Proteins) requires RasGRF1 (show RASGRF1 Proteins)/CaMKII (show CAMK2G Proteins) to alter dendritic spine formation.
Study suggests a complex role of ERK (show EPHB2 Proteins)-dependent and Ras-GRF1 (show RASGRF1 Proteins)-dependent signaling in corticostriatal plasticity, highlights differences between synaptic mechanisms in naive slices and dopamine-depleted preparations from L-DOPA-treated dyskinetic animals
RasGrf1 (show RASGRF1 Proteins) is an important upstream component of signal transduction pathways regulating Pttg1 (show PTTG1 Proteins) expression and controlling beta cell development and physiological responses.
CARD9 (show CARD9 Proteins) regulates H-Ras (show HRAS Proteins) activation by linking Ras-GRF1 (show RASGRF1 Proteins) to H-Ras (show HRAS Proteins), which mediates Dectin-1 (show CLEC7A Proteins)-induced extracellular signal-regulated protein kinase (show CDK7 Proteins) (ERK (show EPHB2 Proteins)) activation and proinflammatory responses when stimulated by their ligands.
GRF1 is expressed in new neurons when GRF1 loss begins to effect neuronal function, promoting late stages of adult neurogenesis. GRF1 is an age-dependent regulator of adult hippocampal neurogenesis and the ability to distinguish closely related contexts.
Data indicate that contextual discrimination involves term potentiation (LTP (show SCP2 Proteins)) promoted by calcium-permeable AMPA (show GRIA3 Proteins)-type glutamate (show GRIN1 Proteins) receptors, RAS-GRF1 (show RASGRF1 Proteins) and p38 MAP kinase (show MAPK14 Proteins).
The cellular RacGAP activity of p190RhoGAP requires an intact polybasic region adjacent to the GAP domain whereas the RhoGAP (show ARHGAP1 Proteins) activity is inhibited by the same domain.
interaction involves the first FF motif of p190A and the winged helix/PCI (show SERPINA5 Proteins) domain of eIF3A (show EIF6 Proteins), is enhanced by serum stimulation and reduced by phosphatase treatment
these data demonstrate that a complex of p190RhoGAP-A and anillin (show ANLN Proteins) modulates RhoA (show RHOA Proteins)-GTP (show AK3 Proteins) levels in the cytokinetic furrow to ensure progression of cytokinesis.
These results place Blk (show BLK Proteins) upstream of the p190RhoGAP-RhoA (show RHOA Proteins) pathway in Galpha13 (show GNA13 Proteins)-activated cells, overall representing an opposing signaling module during CXCL12 (show CXCL12 Proteins)-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 (show RASA1 Proteins)), is expressed in much lower levels in DKO4 cells compared to DLD1, and this expression is regulated by KRAS.
Overexpression of p190 (show CNTNAP1 Proteins) 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 (show RHOA Proteins) 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 (show RHOA Proteins) activity mediated by activating the FR/cSrc/p190RhoGAP-signaling pathway.
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
, rho GTPase-activating protein 35
, P190 RhoGAP
, glucocorticoid receptor DNA-binding factor 1
, GRF beta
, Ras guanine release factor beta
, guanine nucleotide releasing factor 1
, guanine nucleotide-releasing protein
, ras-specific guanine nucleotide-releasing factor 1
, ras-specific nucleotide exchange factor CDC25
, glucocorticoid receptor repression factor 1
, rho GAP p190A
, GAP-associated protein p190