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The oncogenic potential of Ras is activated by point mutations mainly involving the codons 12 and 61, which impair the intrinsic GTPase activity and, moreover, render Ras insensitive to the GAP action, leading to constitutive activation of downstream effectors such as Raf kinases including c-Raf-1 and B-Raf, PI3Ks, and Ral guanine nucleotide dissociation stimulator RalGDS family proteins 1.
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