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. (Shipping Cost: €200.00)

RAS (G12D Mutant Specific) Polyclonal

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.

RAS (G12D Mutant Specific) Polyclonal