
NCBI . NLM . NIH . GOV {
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Title[redir]:
The RAF inhibitor PLX4032 inhibits ERK signaling and tumor cell proliferation in a V600E BRAF-selective manner - PMC
Description:
Tumors with mutant BRAF and some with mutant RAS are dependent upon ERK signaling for proliferation, and their growth is suppressed by MAPK/ERK kinase (MEK) inhibitors. In contrast, tumor cells with human EGF receptor (HER) kinase activation ...
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Keywords {🔍}
erk, cells, doi, plx, cell, tumors, mek, brafve, expression, raf, signaling, google, scholar, mutant, tumor, inhibition, pubmed, inhibitors, fig, genes, braf, lines, output, ras, cancer, induction, kinase, activation, meki, phosphorylation, brafwt, pmc, effects, article, mutation, inhibitor, perk, pathway, growth, feedback, patients, melanoma, skmel, free, inhibits, including, proliferation, data, response, rafi,
Topics {✒️}
extracellular signal-regulated kinase kit/cyclin-dependent kinase-4 overexpression atp-competitive raf-kinase inhibitors proto-oncogene product raf-1 major consulting/advisory roles minor consulting/advisory roles allosteric mapk/erk kinase increased steady-state output average-linkage hierarchical clustering pmc beta search steady-state erk output g2/m-phase subpopulations atp-competitive raf inhibitor genome-wide expression patterns oncogenic b-raf kinase erk-dependent transcriptional output mek-dependent ras-mutant tumors pan-raf inhibitors bind org/lookup/suppl/doi brafwt/raswt cell line mutant braf-selective manner mek/erk-independent manner brafwt/raswt cell lines activated raf kinase supplementary materials included dual-specificity phosphatases brafv600e-mutant cell lines raf-erk signaling pathway mapk/erk kinase supporting information online receptor tyrosine kinase kinase-dead braf small absolute change transactivate raf dimers mek-erk independent mechanism erk transcriptional output publisher site pdf atp-competitive inhibitors mek-dependent gene expression full-time employees important biologic effects heat map representation increased erk output license information pmcid kinase activation proliferate rtk-driven tumor cells activated mutant ras including erk-dependent tumors individual cell line kinase-dependent tumors
Questions {❓}
- What, then, is the potential utility of such an agent, in comparison with MEK inhibitors?
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