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The RAS protein family consists of small GTPases that act as molecular switches in cell signaling pathways, controlling processes such as cell growth, differentiation, and survival. Mutant forms of RAS proteins are among the most common oncogenic drivers in human cancers. The three main RAS genes in humans are KRAS, NRAS, and HRAS. They cycle between an inactive GDP-bound state and an active GTP-bound state, activating downstream signaling pathways when GTP-bound. Oncogenic mutations, frequently found at codons 12, 13, and 61, impair GTPase activity, resulting in constitutive activation and uncontrolled cell proliferation.
Inhibition of mutant RAS protein activity, disruption of RAS interaction with downstream effectors, inhibition of RAS post-translational modifications
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