Ras (E8N8L) XP® Rabbit mAb (BSA and Azide Free) #82819
- WB
- IHC
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 21 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Storage
Specificity / Sensitivity
Ras (E8N8L) XP® Rabbit mAb (BSA and Azide Free) 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.
Limited Uses
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