KRAS <sup>G12C</sup> inhibition produces a driver-limited state revealing collateral dependencies
Kevin Lou(University of California, San Francisco), Luke A. Gilbert(University of California, San Francisco), John D. Gordan(University of California, San Francisco), Christopher Yogodzinski(University of California, San Francisco), Yeonjoo Hwang(UCSF Helen Diller Family Comprehensive Cancer Center), Alex Y. Ge(University of California, San Francisco), Arielle Shkedi(University of California, San Francisco), Kevan M. Shokat(Howard Hughes Medical Institute), Danielle L. Swaney(Gladstone Institutes), D. Mitchell(University of California, San Francisco), Byron Hann(University of California, San Francisco), Alex Choi(University of California, San Francisco), Veronica Steri(University of California, San Francisco)
Cited by 179
Related Papers
K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
|Nature|2013|2.5k
RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF
|Nature|2010|1.8k
IRE1 Signaling Affects Cell Fate During the Unfolded Protein Response
|Science|2007|1.4k