Product Pathways - MAPK Signaling
Ras Antibody #3965
|W||H M R Mk Dm Pg Sc (Hm) (C) (X) (Z) (Dg)||Endogenous||21||Rabbit|
Reactivity Key: H=Human M=Mouse R=Rat Hm=Hamster Mk=Monkey C=Chicken Dm=D. melanogaster X=Xenopus Z=Zebrafish Dg=Dog Pg=Pig Sc=S. cerevisiae
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
Ras Antibody detects endogenous levels of total K-Ras, H-Ras, and N-Ras. This antibody may also cross-react with R-Ras and M-Ras.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues close to the amino-terminus of human K-Ras. Antibodies are purified by protein A and peptide affinity chromatography.
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.