Ras (E8N8L) XP® Rabbit mAb #67648
- WB
- IP
- IHC
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 21 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:50 - 1:250 |
| Immunoprecipitation | 1:50 |
| Immunohistochemistry (Paraffin) | 1:200 - 1:800 |
Storage
For a carrier free (BSA and azide free) version of this product see product #82819.
Protocol
Specificity / Sensitivity
Ras (E8N8L) XP® Rabbit mAb detects endogenous levels of total K-Ras, H-Ras, and N-Ras proteins.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Glu37 of human K-Ras protein.
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.
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