title: Selective Targeting of the KRAS G12C Mutant: Kicking KRAS When It's Down.
abstract: Two recent studies evaluated a small molecule that specifically binds to and inactivates the KRAS G12C mutant. The new findings argue that the perception that mutant KRAS is persistently frozen in its active GTP-bound form may not be accurate.
authors.affiliation: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
authors.forename: G Aaron
authors.initials: GA
authors.lastname: Hobbs
authors.affiliation: Department of Structural Biology, Max Planck Institute of Molecular Physiology, 44227 Dortmund, Germany.
authors.forename: Alfred
authors.initials: A
authors.lastname: Wittinghofer
authors.affiliation: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: cjder@med.unc.edu.
authors.forename: Channing J
authors.initials: CJ
authors.lastname: Der
mesh_terms: D001384:Azetidines; D006153:Guanosine Diphosphate / Q000378:metabolism; D006160:Guanosine Triphosphate / Q000378:metabolism; D006801:Humans; D009154:Mutation / Q000235:genetics*; D010879:Piperazines; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics* / Q000378:metabolism
chemical_list: C000605991:ARS853; D001384:Azetidines; C117307:KRAS protein, human; D010879:Piperazines; D006153:Guanosine Diphosphate; D006160:Guanosine Triphosphate; D016283:Proto-Oncogene Proteins p21(ras)