Render Target: STATIC
Render Timestamp: 2024-12-26T10:54:05.235Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-08-01 15:23:30.147
Product last modified at: 2024-10-08T16:45:09.193Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

p190-B RhoGAP Antibody #2562

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R Mk B
    SENSITIVITY Endogenous
    MW (kDa) 190
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 
    • B-Bovine 

    Product Information

    Product Usage Information

    Application Dilution
    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

    Specificity / Sensitivity

    p190-B RhoGAP Antibody detects endogneous levels of total RhoGAP protein.

    Species Reactivity:

    Human, Mouse, Rat, Monkey, Bovine

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to a region surrounding Lys296 of human p190-B RhoGAP. Antibodies are purified by protein A and 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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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