Application
| WB, IHC, ICC |
|---|---|
| Primary Accession | B2KGV5 |
| Other Accession | NP_035067.2 |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat, Bovine |
| Clonality | Polyclonal |
| Description | Rabbit Anti-Human RAS Polyclonal |
| Target/Specificity | Detects ~21kDa. |
| Other Names | GTPase Hras Antibody, GTPase Kras Antibody, GTPase Nras Antibody, Ha Ras Antibody, K Ras Antibody, K ras p21 Antibody, KRAS Antibody, NRAS Antibody, p21ras Antibody, RASH2 Antibody |
| Immunogen | Synthetic peptide corresponding to amino acids 31-43 of human RAS. (The immunogen peptide is from the effector binding loop (l2) of the H, K and N-Ras (AA31-43). This sequence is identical yeast, slime mould, fungi, Xenopus, rat, mouse and chicken over these residues.) |
| Purification | Protein G Purified |
| Storage | -20ºC |
| Storage Buffer | PBS pH7.4, 50% glycerol, 0.09% sodium azide |
| Shipping Temperature | Blue Ice or 4ºC |
| Certificate of Analysis | 1 µg/ml of SPC-173 was sufficient for detection of Ras in 20 µg of Hela cell lysate by colorimetric immunoblot analysis using goat anti-rabbit IgG:HRP as the secondary antibody. |
| Cellular Localization | Cell Membrane | Golgi Apparatus | Golgi Apparatus Membrane |
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Provided below are standard protocols that you may find useful for product applications.
Background
The 21 kDa guanine-nucleotide binding proteins (K-Ras, H-Ras and N-Ras) cycle between active (GTPbound) 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, 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 Asp (G12D), which prevents Ras inactivation, possibly by increasing the overall rigidity of the protein (5,6).
References
1. Boguski M.S. and McCormick F. (1993) Nature 366: 643–654.
2. Avruch J., et al. (1994) Trends Biochem. Sci.19: 279–283.
3. Buday L. and Downward J. (1993) Cell 73: 611–620.
4. Huang D.C., et al. (1993) Mol. Cell Biol. 13: 2420–2431.
5. Bos J.L. (1989) Cancer Res. 49: 4682–4689.
6. Ma J. and Karplus M. (1997) J. Mol. Biol. 274:114–131.