RAS (G12D Mutant Specific) [HL10]

The guanine-nucleotide binding protein (K-Ras, H-Ras, and N-Ras) is 21 kDa membrane-associated GTPase which cycles between active (GTP-bound) and inactive (GDP-bound) forms, regulates cell proliferation, differentiation, and survival. Receptor tyrosine kinases and G protein-coupled receptors activate Ras, which then stimulates the Raf-MEK-MAPK pathway. GTPase-activating proteins (GAP) normally facilitate the inactivation of Ras. However, studies show that in 30% of human cancers, point mutations in Ras prevent the GAP-mediated inhibition of this pathway. The most common oncogenic Ras mutation is Gly12 to Asp12 (G12D) – Ras missense mutations at the codon 12, which results in decreased GTPase activity and constitutive signaling, possibly by increasing the overall rigidity of the protein. KRAS has the distinction of being a preeminent oncoprotein as it is mutated in more than 85% of RAS-altered cancers. This recombinant clone [HL10] demonstrates exceptional specificity for the RAS G12D mutant protein.