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The 21 kDa guanine-nucleotide binding proteins (K-Ras,
H-Ras and N-Ras) cycle between active (GTPbound)
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 (GAP) normally facilitate the inactivation
of Ras. However, 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 Asp (G12D),
which prevents Ras inactivation, possibly by increasing
the overall rigidity of the protein (5,6).