Article
KRASG12C inhibition produces a driver-limited state revealing collateral dependencies.
Science signaling - 28 May 2019
Lou Kevin, Steri Veronica, Ge Alex Y, Hwang Y Christina, Yogodzinski Christopher H, Shkedi Arielle R, Choi Alex L M, Mitchell Dominique C, Swaney Danielle L, Hann Byron, Gordan John D, Shokat Kevan M, Gilbert Luke A
Abstract excerpt
Inhibitors targeting KRASG12C, a mutant form of the guanosine triphosphatase (GTPase) KRAS, are a promising new class of oncogene-specific therapeutics for the treatment of tumors driven by the mutant protein. These inhibitors react with the mutant cysteine residue by binding covalently to the switch-II pocket (S-IIP) that is present only in the inactive guanosine diphosphate (GDP)-bound form of KRASG12C, sparing...
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