Product Pathways - Cytoskeletal Signaling
p190-A RhoGAP (C59F7) Rabbit mAb #2860
|2860S||100 µl (10 western blots)||---||In Stock||---|
|2860||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Hamster, Monkey||Endogenous||190||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation
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 blot analysis of extracts from various cell types using p190-A RhoGAP (C59F7) Rabbit mAb.
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).
- Peck, J. et al. (2002) FEBS Lett. 528, 27-34.
- Moon, S.Y. and Zheng, Y. (2003) Trends Cell Biol. 13, 13-22.
- Wang, Z. et al. (1996) Cell Growth Differ 7, 123-33.
- Tikoo, A. et al. (2000) Gene 257, 23-31.
- Jiang, W. et al. (2005) Mol Cell 17, 23-35.
- Wolf, R.M. et al. (2003) Genes Dev 17, 476-87.
- Su, L. et al. (2003) J Cell Biol 163, 571-82.
- Sordella, R. et al. (2002) Dev Cell 2, 553-65.
- Sordella, R. et al. (2003) Cell 113, 147-58.
- Chang, J.H. et al. (1995) J Cell Biol 130, 355-68.
- Roof, R.W. et al. (1998) Mol Cell Biol 18, 7052-63.
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For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
This antibody is developed, validated, and produced by CST using in part technology under license (granting certain rights including those under U.S. Patent No. 5,675,063) from Epitomics, Inc.