Lactylation of Mutation-Prone RAS Residues Mimics Oncogenic Mutations and Drives Constitutive Activation.

Abstract excerpt

Background: Elevated expression of wild-type RAS contributes to tumorigenesis, yet the mechanisms underlying its mutation-independent hyperactivity remain unclear. Lactylation, a lactate-derived post-translational modification, has emerged as a regulator in cancer, but its role in RAS activation is unknown. Here, we investigated whether lactylation of RAS at specific residues drives its constitutive activation...

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