Product Pathways - MAPK Signaling
Ras (D2C1) Rabbit mAb #8955
|W||H M R Mk||Endogenous||21||Rabbit IgG|
Reactivity Key: H=Human M=Mouse R=Rat Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
Ras (D2C1) Rabbit mAb recognizes endogenous levels of total Ras protein, specifically K-Ras and N-Ras. This antibody does not cross-react with H-Ras or R-Ras.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a recombinant protein specific to human K-Ras protein.
The 21 kDa guanine-nucleotide binding proteins (K-Ras, H-Ras, and N-Ras) cycle between active (GTP-bound) and inactive (GDP-bound) forms (1). Receptor tyrosine kinases and G protein-coupled receptors activate Ras, which then stimulates the Raf-MEK-MAPK pathway (2-4). GTPase-activating proteins (GAP) normally facilitate the inactivation of Ras. However, research studies have shown that in 30% of human tumors, point mutations in Ras prevent the GAP-mediated inhibition of this pathway (5). The most common oncogenic Ras mutation found in tumors is Gly12 to Asp12 (G12D), which prevents Ras inactivation, possibly by increasing the overall rigidity of the protein (5,6).
- Boguski, M.S. and McCormick, F. (1993) Nature 366, 643-654.
- Avruch, J. et al. (1994) Trends Biochem. Sci. 19, 279-283.
- Buday, L. and Downward, J. (1993) Cell 73, 611-620.
- Huang, D.C. et al. (1993) Mol. Cell Biol. 13, 2420-2431.
- Bos, J.L. (1989) Cancer Res. 49, 4682-4689.
- Ma, J. and Karplus, M. (1997) J. Mol. Biol. 274, 114-131.
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For Research Use Only. Not For Use In Diagnostic Procedures.