K-Ras Antibody #33197
Filter:
- WB
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with constructs expressing full-length human K-Ras (hK-Ras; +) or full-length human N-Ras (hN-Ras; +), using K-Ras Antibody (upper), Ras (27H5) Rabbit mAb #3339 (middle), or β-Actin (D6A8) Rabbit mAb #8457 (lower).
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 21 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Related Products
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
K-Ras Antibody recognizes endogenous levels of total K-Ras protein. This antibody cross-reacts with N-Ras in a K-Ras preferred manner, but does not cross-react with H-Ras or R-Ras protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val125 of human K-Ras protein. Antibodies are purified by peptide affinity chromatography.
Background
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 (GAPs) 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, 643-54.
- Avruch, J. et al. (1994) Trends Biochem Sci 19, 279-83.
- Buday, L. and Downward, J. (1993) Cell 73, 611-20.
- Huang, D.C. et al. (1993) Mol Cell Biol 13, 2420-31.
- Bos, J.L. (1989) Cancer Res 49, 4682-9.
- Ma, J. and Karplus, M. (1997) J Mol Biol 274, 114-31.
Pathways
Explore pathways related to this product.
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