The 21 kDa guanine-nucleotide binding proteins (K-Ras, H-Ras and N-Ras) cycle between active (GTP-bound) and inactive (GDP-bound) forms. 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, in 30% of human tumors, point mutations in Ras prevent the GAP-mediated inhibition of this pathway. 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.
HRAS; v-Ha-ras Harvey rat sarcoma viral oncogene homolog; HRAS1; GTPase HRas; p21ras; H-Ras-1; p19 H-RasIDX protein; c-has/bas p21 protein; transforming protein p21; Ha-Ras1 proto-oncoprotein; c-ras-Ki-2 activated oncogene; GTP- and GDP-binding peptide B; transformation gene: oncogene HAMSV; Ras family small GTP binding protein H-Ras; CTLO; HAMSV; K-RAS; N-RAS; RASH1; C-H-RAS; H-RASIDX; C-BAS/HAS; C-HA-RAS1; Harvey rat sarcoma viral oncogene homolog; H-RAS; v-Ha-ras Harvey rat sarcoma viral oncogene-like protein