CST, 2513S, p190-A RhoGAP Antibody

Polyclonal Antibody for studying GRLF1. Validated for Western Blotting. Highly specific and rigorously validated in-house, p190-A RhoGAP Antibody (CST #2513) is ready to ship. Product Usage Information Western Blotting: 1:1000 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting Specificity / Sensitivity p190-A RhoGAP Antibody detects endogenous levels of total p190-A RhoGAP protein (GRLF1). Species Reactivity: Human, Mouse, Rat, Hamster Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to central residues of human p190-A RhoGAP. Antibodies are purified by peptide affinity chromatography. Background Rho family GTPases are key regulators of diverse processes such as cytoskeletal organization, cell growth and differentiation, transcriptional regulation, and cell adhesion/motility. The activities of these proteins are controlled primarily through guanine nucleotide exchange factors (GEFs) that facilitate the exchange of GDP for GTP, promoting the active (GTP-bound) state, and GTPase activating proteins (GAPs) that promote GTP hydrolysis and the inactive (GDP-bound) state (1,2). The p190 RhoGAP proteins are widely expressed Rho family GAPs. p190-A has been characterized as a tumor suppressor, and research studies have shown that loss or rearrangement of the chromosomal region containing the gene for p190-A is linked to tumor development (3,4). p190-A binds the mitogen-inducible transcription factor TFII-I, sequestering it in the cytoplasm and inhibiting its activity. Phosphorylation of p190-A at Tyr308 reduces its affinity for TFII-I, relieving the inhibition (5). p190-A can also inhibit growth factor-induced gliomas in mice (6) and affect cleavage furrow formation and cytokinesis in cultured cells (7). Mice lacking p190-B RhoGAP show excessive Rho activation and a reduction in activation of the transcription factor CREB (8). Cells deficient in p190-B display defective adipogenesis (9). There is increasing evidence that p190 undergoes tyrosine phosphorylation, which activates its GAP domain (9-11). Levels of tyrosine phosphorylation are enhanced by Src overexpression (10,11). IGF-I treatment downregulates Rho through phosphorylation and activation of p190-B RhoGAP, thereby enhancing IGF signaling implicated in adipogenesis (9). Alternate Names ARHGAP35; glucocorticoid receptor DNA binding factor 1; Glucocorticoid receptor DNA-binding factor 1; Glucocorticoid receptor repression factor 1; GRF-1; GRF1; GRLF1; KIAA1722; MGC10745; p190-A; P190A; p190ARhoGAP; p190RhoGAP; RHG35; Rho GAP p190A; Rho GTPase activating protein 35; Rho GTPase-activating protein 35 Specification REACTIVITY: H M R Hm SENSITIVITY: Endogenous MW (kDa): 190 SOURCE: Rabbit