Regulation of Raf-1 by direct feedback phosphorylation.

By M. Dougherty, Jurgen Müller, Daniel A. Ritt, Ming Zhou, X. Zhou, T. Copeland, Thomas P. Conrads, Timothy D. Veenstra, K. Lu, D. Morrison. Molecules and Cells, 2005

650 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/16e52893880136bb245c8ff2bb28a8e7fc443bdb

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Citations in the corpus

Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “Negative feedback signals for Ras have been reported by means of ERK-mediated phosphorylatio”
Phosphatase‐mediated crosstalk between MAPK signaling pathways in the regulation of cell survival (2008, background): “Similarly, PP2A, along with the prolyl isomerase Pin1, were shown to cooperate in dephosphorylating Raf-1 on critical inhibitory sites that prevent Raf-1 reactivation (101).”
Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging (2011, background): “Depending upon the site phosphorylated on Raf-1, ERK phosphorylation can either enhance [14] or inhibit [15] Raf-1 activity.”
V600EBRAF is associated with disabled feedback inhibition of RAF–MEK signaling and elevated transcriptional output of the pathway (2009, background): “Feedback is mediated by induction of expression of proteins such as Sprouty (22) and the MAPK phosphatases [DUSPs (21)] and by direct phosphorylation and inhibition of proteins like RAF-1 (35).”
Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity (2008, result): “This observation is consistent with previous reports of a negative feedback pathway from ERK through c-Raf-1 (13, 19).”
The prolyl isomerase PIN1: a pivotal new twist in phosphorylation signalling and disease (2007, background): “Furthermore, PIN1 also suppresses a negative feedback mechanism of Ras by promoting the dephosphorylation and, therefore, the activation of Raf, a downstream effector of Ra”
Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State. (2016, methodology): “coli as truncated (1-169), hexahistidine-tagged forms as described by Ostrem and colleagues ( 6 ).”
An Integrated Mechanistic Model of Pan-Cancer Driver Pathways Predicts Stochastic Proliferation and Death (2017, background): “G) ROC curves predicting proliferation from 400 simulated cells (200 training/200 validation) following EGF+ins from initial BRaf and CRaf levels (blue-AUC=0.81; red-AUC=0.74; yellow-AUC=0.69; purple-AUC=0.51).”
Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “Furthermore, serine residues 29, 43, 289, 296, 301, and 642 have been reported as ERK-catalyzed phosphorylation sites, which are associated with feedback inhibition [197].”
Differential regulation and properties of MAPKs (2007, background): “Therefore, PP2A activity is required for activation of the pathway (Dougherty et al., 2005).”
Feedback regulation of EGFR signalling: decision making by early and delayed loops (2011, background): “ERKs mediate negative feedback regulation by phosphorylating multiple residues in RAF1, thereby desensitizing it to further stimulatio”
MAP kinase signalling pathways in cancer (2007, background): “Activated ERK can inhibit Raf-1 by direct phosphorylation (Dougherty et al., 2005).”
Discovery of a novel ERK inhibitor with activity in models of acquired resistance to BRAF and MEK inhibitors. (2013, background): “Thereafter, a loss of ERK-mediated inhibitory CRAF phosphorylation (S289/S296/S301) (15) was observed as well as dramatic increases in pERK.”
Prolyl cis-trans isomerization as a molecular timer. (2007, background): “Furthermore, activation of MAP kinases also leads to phosphorylation of Raf to inactivate Raf in a negative feedback loo”