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Mutant Ras proteins are altered forms of the Ras family of small GTPases that are constitutively activated due to mutations, most commonly at codons 12, 13, or 61. These mutations impair GTP hydrolysis, leading to persistent activation of downstream signaling pathways, particularly the RAF-MEK-ERK/MAPK pathway, driving uncontrolled cell growth and contributing to cancer development. The three main isoforms are HRAS, KRAS, and NRAS, each playing distinct roles in different cancer types. Therapeutic strategies focus on direct or indirect inhibition of mutant Ras, as well as targeting downstream effectors and post-translational modifications.
Inhibition of mutant Ras activity, inhibition of downstream signaling pathways, inhibition of post-translational modifications required for Ras function
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