SHOC2 and CRAF Mediate ERK1/2 Reactivation in Mutant NRAS-mediated Resistance to RAF Inhibitor

ERK1/2 signaling is frequently dysregulated in tumors through BRAF mutation. Targeting mutant BRAF with vemurafenib frequently elicits therapeutic responses; however, durable effects are often limited by ERK1/2 pathway reactivation via poorly defined mechanisms. We generated mutant BRAFV600E melanom...

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Veröffentlicht in:	The Journal of biological chemistry 2012-12, Vol.287 (50), p.41797-41807
Hauptverfasser:	Kaplan, Fred M., Kugel, Curtis H., Dadpey, Neda, Shao, Yongping, Abel, Ethan V., Aplin, Andrew E.
Format:	Artikel
Sprache:	eng
Schlagworte:	Amino Acid Substitution BRAF Cell Line, Tumor Cell Signaling Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics Enzyme Activation - drug effects Enzyme Activation - genetics Humans Indoles - pharmacology Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - genetics MAP Kinases (MAPKs) Melanoma Mitogen-Activated Protein Kinase 1 - genetics Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - genetics Mitogen-Activated Protein Kinase 3 - metabolism Mutation, Missense NRAS PLX4032 PLX4720 Proto-Oncogene Proteins B-raf - genetics Proto-Oncogene Proteins B-raf - metabolism Proto-Oncogene Proteins c-raf - genetics Proto-Oncogene Proteins c-raf - metabolism Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors Proto-Oncogene Proteins p21(ras) - genetics Proto-Oncogene Proteins p21(ras) - metabolism Raf Ras S Phase - drug effects S Phase - genetics SHOC2 Signal Transduction Sulfonamides - pharmacology
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