Associated Papers
DA-Raf synergistically binds to the plasma membrane and Ras to suppress ERK signaling.
Takano K et al.
Life Science Alliance, 2025
A recurrent de novo damaging variant in EMP2 causes progressive symmetric erythrokeratoderma.
Jiang X et al.
Proceedings of the National Academy of Sciences of the United States of America, 2025
Characterization of MEK1/2 Degraders Uncovers a Kinase-Independent Role for MEK1/2 in the Stabilization and Maturation of CRAF.
Wasserman JS et al.
Biorxiv : the Preprint Server for Biology, 2025
Approaches to Evaluate Whole Exome Sequencing Data That Incorporate Genetic Intolerance Scores for Congenital Anomalies, Including Intronic Regions Adjacent to Exons.
Taniguchi K et al.
Molecular Genetics & Genomic Medicine, 2025
From bench to bedside: murine models of inherited and sporadic brain arteriovenous malformations.
Ricciardelli AR et al.
Angiogenesis, 2025
In-cell single-molecule FRET measurement of cytosolic RAF proteins to investigate the structural states and kinetics among them.
Okamoto K et al.
Frontiers in Molecular Biosciences, 2025
Bioluminescence Resonance Energy Transfer (BRET)-based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells.
Spencer-Smith R
Journal of Visualized Experiments : Jove, 2024
Novel therapeutic perspectives in Noonan syndrome and RASopathies.
Saint-Laurent C et al.
European Journal of Pediatrics, 2024
Genomic analysis of plasma circulating tumor DNA in patients with heavily pretreated HER2 + metastatic breast cancer.
Lee K et al.
Scientific Reports, 2023
Two Closed Conformations of CRAF Require the 14-3-3 Binding Motifs and Cysteine-Rich Domain to be Intact in Live Cells.
Okamoto K et al.
Journal of Molecular Biology, 2023
ARAF protein kinase activates RAS by antagonizing its binding to RASGAP NF1.
Su W et al.
Molecular Cell, 2022
Development and physiological functions of the lymphatic system: insights from human genetic studies of primary lymphedema.
Martin-Almedina S et al.
Physiological Reviews, 2021
Metabolic flexibility maintains proliferation and migration of FGFR signaling-deficient lymphatic endothelial cells.
Song H et al.
The Journal of Biological Chemistry, 2021
Drosophila RASopathy models identify disease subtype differences and biomarkers of drug efficacy.
Das TK et al.
Iscience, 2021
Inhibition of RAF dimers: it takes two to tango.
Cook FA et al.
Biochemical Society Transactions, 2021
CRAF mutations in lung cancer can be oncogenic and predict sensitivity to combined type II RAF and MEK inhibition.
Noeparast A et al.
Oncogene, 2019
SHOC2 complex-driven RAF dimerization selectively contributes to ERK pathway dynamics.
Boned Del Río I et al.
Proceedings of the National Academy of Sciences of the United States of America, 2019
SHOC2 phosphatase-dependent RAF dimerization mediates resistance to MEK inhibition in RAS-mutant cancers.
Jones GG et al.
Nature Communications, 2019
CHAPLE syndrome uncovers the primary role of complement in a familial form of Waldmann's disease.
Ozen A
Immunological Reviews, 2019
Analytical Validation of a Hybrid Capture-Based Next-Generation Sequencing Clinical Assay for Genomic Profiling of Cell-Free Circulating Tumor DNA.
Clark TA et al.
The Journal of Molecular Diagnostics : Jmd, 2018
Metabolic stress regulates ERK activity by controlling KSR-RAF heterodimerization.
Verlande A et al.
Embo Reports, 2018
A computationally engineered RAS rheostat reveals RAS-ERK signaling dynamics.
Rose JC et al.
Nature Chemical Biology, 2017
Reproducible Analysis of Post-Translational Modifications in Proteomes--Application to Human Mutations.
Holehouse AS et al.
Plos One, 2015
Proteome-wide analysis of human disease mutations in short linear motifs: neglected players in cancer?
Uyar B et al.
Molecular Biosystems, 2014
Targeting RAF kinases for cancer therapy: BRAF-mutated melanoma and beyond.
Holderfield M et al.
Nature Reviews. Cancer, 2014
Structure-energy-based predictions and network modelling of RASopathy and cancer missense mutations.
Kiel C et al.
Molecular Systems Biology, 2014
Oncogenic and sorafenib-sensitive ARAF mutations in lung adenocarcinoma.
Imielinski M et al.
The Journal of Clinical Investigation, 2014
Endothelial ERK signaling controls lymphatic fate specification.
Deng Y et al.
The Journal of Clinical Investigation, 2013
Disorders of dysregulated signal traffic through the RAS-MAPK pathway: phenotypic spectrum and molecular mechanisms.
Tartaglia M et al.
Annals of the New York Academy of Sciences, 2010
Impaired binding of 14-3-3 to C-RAF in Noonan syndrome suggests new approaches in diseases with increased Ras signaling.
Molzan M et al.
Molecular and Cellular Biology, 2010
Spry2 does not directly modulate Raf-1 kinase activity in v-Ha-ras-transformed NIH 3T3 fibroblasts.
Ahn JH et al.
Bmb Reports, 2010
Noonan syndrome: clinical aspects and molecular pathogenesis.
Tartaglia M et al.
Molecular Syndromology, 2010
Calmodulin modulates H-Ras mediated Raf-1 activation.
Moretó J et al.
Cellular Signalling, 2008
Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy.
Pandit B et al.
Nature Genetics, 2007
A phosphatase holoenzyme comprised of Shoc2/Sur8 and the catalytic subunit of PP1 functions as an M-Ras effector to modulate Raf activity.
Rodriguez-Viciana P et al.
Molecular Cell, 2006
Identification of novel in vivo Raf-1 phosphorylation sites mediating positive feedback Raf-1 regulation by extracellular signal-regulated kinase.
Balan V et al.
Molecular Biology of the Cell, 2006
Ras binding opens c-Raf to expose the docking site for mitogen-activated protein kinase kinase.
Terai K et al.
Embo Reports, 2005
Regulation of Raf-1 by direct feedback phosphorylation.
Dougherty MK et al.
Molecular Cell, 2005
Raf-1 activation disrupts its binding to keratins during cell stress.
Ku NO et al.
The Journal of Cell Biology, 2004
Dynamic changes in C-Raf phosphorylation and 14-3-3 protein binding in response to growth factor stimulation: differential roles of 14-3-3 protein binding sites.
Hekman M et al.
The Journal of Biological Chemistry, 2004
Regulation of Raf through phosphorylation and N terminus-C terminus interaction.
Chong H et al.
The Journal of Biological Chemistry, 2003
Protein phosphatase 2A positively regulates Ras signaling by dephosphorylating KSR1 and Raf-1 on critical 14-3-3 binding sites.
Ory S et al.
Current Biology : Cb, 2003
Protein kinase A blocks Raf-1 activity by stimulating 14-3-3 binding and blocking Raf-1 interaction with Ras.
Dumaz N et al.
The Journal of Biological Chemistry, 2003
Mutations in conserved regions 1, 2, and 3 of Raf-1 that activate transforming activity.
Chan EY et al.
Molecular Carcinogenesis, 2002
Dephosphorylation of Ser-259 regulates Raf-1 membrane association.
Kubicek M et al.
The Journal of Biological Chemistry, 2002
Regulation of Raf-1 activation and signalling by dephosphorylation.
Dhillon AS et al.
The Embo Journal, 2002
Protein phosphatases 1 and 2A promote Raf-1 activation by regulating 14-3-3 interactions.
Jaumot M et al.
Oncogene, 2001