RAS proteins have weak intrinsic GTPase activity in the absence of other effectors (Gibbs et al, 1984; reviewed in Pylayeva-Gupta et al, 2011). Nucleotide attack is mediated by residue Q61 and facilitated by van der Waals bonds contributed by glycine residues at position 12 and 13; these three residues account for the majority of oncogenic and pathogenic mutations found in RAS proteins (reviewed in Prior et al, 2012). GAP proteins stimulate the intrinsic GTPase activity of RAS proteins by inserting an arginine residue into the active site, which contributes to proper positioning of the critical Q61 RAS residue (reviewed in King et al, 2013).
King, PD, Lubeck, BA, Lapinski, PE
Pylayeva-Gupta, Y, Grabocka, E, Bar-Sagi, D
Prior, IA, Lewis, PD, Mattos, C
Gibbs, JB, Sigal, IS, Poe, M, Scolnick, EM
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