RAS GTPase family (mutated forms) (RAS (mutated))

Mutated RAS refers to oncogenic variants of the RAS GTPase family proteins (KRAS, NRAS, HRAS), which cycle between inactive GDP-bound and active GTP-bound states to regulate signaling pathways. Common mutations at G12, G13, Q61 impair GTP hydrolysis by disrupting GAP binding, locking RAS in the GTP-bound active state and driving tumorigenesis through effector pathways like MAPK/RAF and PI3K. These mutants exhibit allele-specific structural changes in switch I/II regions, altering nucleotide exchange, effector affinity (e.g., PI3Kα), and transforming potential, with KRAS most frequently mutated in cancers.[1][2][6][8][10] "Mutated RAS" is not a specific single target but a broad class, hence flagged as incorrect for precise targeting; specific isoforms/mutants (e.g., KRAS G12C) are therapeutically addressed.[1][2][9]

Other names

Mutated RASoncogenic RASRAS mutantsKRAS mutantsNRAS mutantsHRAS mutantsRAS proto-oncogenes (mutated)

Covalent binding to mutant cysteine (e.g., G12C), GAP disruption preventing GTP hydrolysis, Stabilization of inactive conformations, Inhibition of effector interactions (e.g., RAF dimerization)