The RAF proteins take centre stage

By C. Wellbrock, M. Karasarides, R. Marais. Nature reviews. Molecular cell biology, 2004

1,252 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/16e82ada15b7299fb5794ef5fe056f3b6c1ffd35

How researchers see this paper

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

In Computational Theory and Mathematics

1. Walter Kolch

In Molecular Biology

1. Peter W. Laird
2. R. Seger
3. C. Der
4. D. Morrison
5. Walter Kolch
6. Yoav D. Shaul
7. P. Roberts
8. M. McKay

Citations in the corpus

• BRafV600E cooperates with Pten silencing to elicit metastatic melanoma (2009, background): “Although it contributes to the aberrant pathophysiological characteristics of the melanoma cel”
• The RAS/RAF/MEK/ERK and the PI3K/AKT signalling pathways: role in cancer pathogenesis and implications for therapeutic approaches (2012, background): “BRAF mutations occur in approximately 8% of human carcinomas, most frequently in melanoma (41%), thyroid (45%) and colorectal (14%) cancers [23,26].”
• Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update. (2012, background): “The paradigm of Raf regulation points to three crucial events governing MAP3K activation: 1) binding to an upstream activating protein and consequent membrane translocation, 2) phosphorylation, and 3) homoligomerization (236, 317, 350).”
• The 14-3-3 proteins: integrators of diverse signaling cues that impact cell fate and cancer development (2008, background): “Under normal signaling conditions, this heterodimerization of C- and B-Raf occurs in response to Ras activation and promotes maximal activation of C-Raf (Figure 1a).”
• Integrating signals from RTKs to ERK/MAPK (2007, background): “Strikingly, converting the Raf kinases from inactive to active enzymes is a highly complex process, involving membrane localization, cycles of phosphorylation/dephosphorylation and protein interactions (Figure 2; reviewed in Dhillon and Kolch, 2002; Wellbrock et al., 2004).”
• Melanoma biology and new targeted therapy (2007, background): “Ras/Raf/MEK/ERK signalling The Ras/Raf/MEK/ERK pathway regulates cell fate decisions downstream of receptor tyrosine kinases, cytokines and heterotrimeric G-protein-coupled receptor”
• RAF inhibitors transactivate RAF dimers and ERK signaling in cells with wild-type BRAF (2010, neutral): “Phosphorylation of CRAF at S338 and S621 has been correlated with its activation 7 .”
• RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E) (2011, background): “ppt"/> Activated RAS promotes dimerization of members of the RAF kinase famil”
• Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy (2007, background): “Finally, we determined the status of 14-3-3 binding, which is mediated through Ser259 and Ser621 when they are phosphorylated and is important for the regulation of RAF1 (ref”
• The MEK/ERK cascade: from signaling specificity to diverse functions. (2007, background): “Ras), which transmit the signal further by recruiting the MAP3K tier Raf kinases to the plasma membrane, where they are activated [10].”
• MAP kinase signalling pathways in cancer (2007, background): “As the literature on MAPK pathways and cancer is huge and includes comprehensive recent reviews (Downward, 2003; Wellbrock et al., 2004; Kolch, 2005; Bradham and McClay, 2006; Galabova-Kovacs et al., 2006; Kohno and Pouyssegur, 2006; Torii et al., 2006), we will take the liberty of a more…”
• Phosphatase‐mediated crosstalk between MAPK signaling pathways in the regulation of cell survival (2008, background): “In addition, mutations of B-Raf, which increase the activity of the MEK1,2ERK1,2 pathway, were found in several malignancies and expression of such mutants in NIH3T3 cells lead to transformation (11, 20).”
• Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer (2007, background): “Targeting the Raf-MEK-ERK MAPK cascade PJ Roberts and CJ Der A-Raf and B-Raf) (Wellbrock et al., 2004; Schreck and Rapp, 2006).”
• Hyperactive Ras in developmental disorders and cancer (2007, background): “The finding that germline BRAF mutations underlie most cases of CFC syndrome is of exceptional interest to cancer biologists because, as discussed below, a V600E substitution in BRAF is one of the most common molecular lesions found in human cance”