V600EBRAF is associated with disabled feedback inhibition of RAF–MEK signaling and elevated transcriptional output of the pathway

By C. Pratilas, Barry S. Taylor, Q. Ye, A. Viale, Christopher Sander, D. Solit, N. Rosen. Proceedings of the National Academy of Sciences of the United States of America, 2009

616 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7923fc90521c0b570b6d6e15178115a7fa3f04d7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

Citations in the corpus

An Integrated Approach to Uncover Drivers of Cancer (2010, methodology): “We usedGSEA tomeasure enrichment of an experimentally derived set of genes that respond to MEK inhibition in melanoma (Pratilas et al., 2009).”
Resistance to vemurafenib resulting from a novel mutation in the BRAFV600E kinase domain (2013, methodology): “First, we monitored expression of three representative ERK target genes (FOSL1, SPRY2, and DUSP6), a biologically relevant output of the BRAFMEK-ERK signaling pathway (Pratilas et al., 2009).”
AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity (2011, positive): “It is increasingly clear that dysregulation of mitogenic signaling by constitutively activated oncoproteins in cancer cells drives high levels of feedback inhibition of the signaling network (Courtois-Cox et al., 2006; O’Reilly et al., 2006; Pratilas et al., 2009).”
MEK1 mutations confer resistance to MEK and B-RAF inhibition (2009, background): “2C), consistent with modulation of feedback inhibition (19).”
Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies (2023, background): “This ﬁ gure was created with BioRender.com kinase pathway.”
Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF (2013, positive): “(B) Effects of MEK inhibitor PD0325901 on MITF mRNA and MITF targets by published microarray (Pratilas et al., 2009).”
Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State. (2016, methodology): “Protein expression and purification: KRAS-G12C, WT, and G13C proteins were expressed in E coli as truncated (1-169), hexahistidine tagged forms as described by Ostrem et al(6).”
Integrated Genomic Characterization of Papillary Thyroid Carcinoma (2014, methodology): “Conversely, tumors driven by RAS and RTK fusions signal via RAF dimers that respond to ERK feedback, resulting in lower MAPK-signaling.”