Cell Signaling Technology

Product Pathways - Cytoskeletal Signaling

p190-B RhoGAP Antibody #2562

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk B Endogenous 190 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  B=Bovine
Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

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

Source / Purification

Polyclonal antibodies are produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to a region surrounding Lys296 of human p190-B RhoGAP. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot anlaysis of extracts from MCF-7 (human), C2C12 (mouse), and BAEC (bovine) cells, using p190-B RhoGAP Antibody.

Background

The Rho family of small GTPases, including Rho, Rac and Cdc42, are key regulators of diverse biological processes such as cytoskeletal organization, cell growth and differentiation, transcriptional regulation, and cell adhesion/motility (1,2). The activities of these proteins are controlled by GTP binding such that in the GTP-bound state they are active, and in the GDP-bound state they become inactive. Three classes of regulatory proteins control the activity of the GTPases by balancing the levels of GTP/GDP binding: the guanine nucleotide exchange factors (GEFs), which promote the active state by facilitating the exchange of GDP for GTP; the guanine nucleotide dissociation inhibitors (GDIs), which sequester the GDP-bound forms and may regulate their intracellular localization; and the GTPase activating proteins (GAPs), which increase GTP hydrolysis to promote the inactive state. The p190 RhoGAP family consists of two related proteins, p190-A and p190-B, which are both widely expressed and contain an amino-terminal GTPase domain and a carboxy-terminal RhoGAP catalytic domain. Mice lacking p190-B RhoGAP show excessive Rho activation and a reduction in activation of the transcription factor CREB (3). Phenotypes of these mice are similar to those of CREB knockouts, with reduced cell size, as well as defects in thymus and neural development (3). Cells deficient in p190-B also display defective adipogenesis, suggesting this pathway is critical for the "adipogenesis-myogenesis switch." (4). There is increasing evidence that p190 undergoes tyrosine phosphorylation, which activates its GAP domain (4-6). Levels of tyrosine phosphorylation are enhanced by Src overexpression (5,6). IGF-1 treatment downregulates Rho through phosphorylation and activation of p190-B RhoGAP, thereby enhancing IGF signaling implicated in adipogenesis (4).

  1. Peck, J. et al. (2002) FEBS Lett. 528, 27-34.
  2. Moon, S.Y. and Zheng, Y. (2003) Trends Cell Biol. 13, 13-22.
  3. Sordella, R. et al. (2002) Dev. Cell 2, 553-565.
  4. Sordella, R. et al. (2003) Cell 113, 147-158.
  5. Chang, J. H. et al. (1995) J. Cell. Biol. 130, 355-368.
  6. Roof, R. W. et al. (1998) Mol. Cell. Biol. 18, 7052-7063.

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This product is for in vitro research use only and is not intended for use in humans or animals. This product is not intended for use as therapeutic or in diagnostic procedures.

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