Cell Signaling Technology

Product Pathways - Cytoskeletal Signaling

p190-A RhoGAP (C59F7) Rabbit mAb #2860

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H M R Hm Mk Endogenous 190 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  Hm=Hamster  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

p190-A RhoGAP (C59F7) Rabbit mAb detects endogenous levels of total p190-A RhoGAP protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human p190-A RhoGAP.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell types using p190-A RhoGAP (C59F7) Rabbit mAb.

IP

IP

Immunoprecipitation of p190-A RhoGAP from CHO cell extracts using p190-A RhoGAP (C59F7) Rabbit mAb. Western blot detection was performed using the same antibody. Lane 1 is 5% input.

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).

  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. Wang, Z. et al. (1996) Cell Growth Differ 7, 123-33.
  4. Tikoo, A. et al. (2000) Gene 257, 23-31.
  5. Jiang, W. et al. (2005) Mol Cell 17, 23-35.
  6. Wolf, R.M. et al. (2003) Genes Dev 17, 476-87.
  7. Su, L. et al. (2003) J Cell Biol 163, 571-82.
  8. Sordella, R. et al. (2002) Dev Cell 2, 553-65.
  9. Sordella, R. et al. (2003) Cell 113, 147-58.
  10. Chang, J.H. et al. (1995) J Cell Biol 130, 355-68.
  11. Roof, R.W. et al. (1998) Mol Cell Biol 18, 7052-63.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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