Ras (E8N8L) Rabbit mAb

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). 1.Boguski, M.S. and McCormick, F. (1993) Nature 366, 643-54. 2.Avruch, J. et al. (1994) Trends Biochem Sci 19, 279-83. 3.Buday, L. and Downward, J. (1993) Cell 73, 611-20. 4.Huang, D.C. et al. (1993) Mol Cell Biol 13, 2420-31. 5.Bos, J.L. (1989) Cancer Res 49, 4682-9. 6.Ma, J. and Karplus, M. (1997) J Mol Biol 274, 114-31.