PNAS

Oncogenic and RASopathy-associated K-RAS mutations relieve membrane-dependent occlusion of the effector-binding site [Biophysics and Computational Biology]

M. T. Mazhab-Jafari, C. B. Marshall, M. J. Smith, G. M. C. Gasmi-Seabrook, P. B. Stathopulos, F. Inagaki, L. E. Kay, B. G. Neel, M. Ikura.
K-RAS4B (Kirsten rat sarcoma viral oncogene homolog 4B) is a prenylated, membrane-associated GTPase protein that is a critical switch for the propagation of growth factor signaling pathways to diverse effector proteins, including rapidly accelerated fibrosarcoma (RAF) kinases and RAS-related protein guanine nucleotide dissociation stimulator (RALGDS) proteins. Gain-of-function KRAS mutations occur...