BRAF Mutants Evade ERK-Dependent Feedback by Different Mechanisms that Determine Their Sensitivity to Pharmacologic Inhibition

ERK signaling requires RAS-induced RAF dimerization and is limited by feedback. Activated BRAF mutants evade feedback inhibition of RAS by either of two mechanisms. BRAF V600 mutants are activated monomers when RAS activity is low; all other activating BRAF mutants function as constitutive RAS-indep...

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Veröffentlicht in:	Cancer cell Jg. 28; H. 3; S. 370
Hauptverfasser:	Yao, Zhan, Torres, Neilawattie M, Tao, Anthony, Gao, Yijun, Luo, Lusong, Li, Qi, de Stanchina, Elisa, Abdel-Wahab, Omar, Solit, David B, Poulikakos, Poulikos I, Rosen, Neal
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States 14.09.2015
Schlagworte:	Cell Line, Tumor Dimerization Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics Humans MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - genetics Mutation - genetics Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins B-raf - antagonists & inhibitors Proto-Oncogene Proteins B-raf - genetics ras Proteins - genetics
ISSN:	1878-3686, 1878-3686
Online-Zugang:	Weitere Angaben
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