ArticleeLife2023
Unveiling the domain-specific and RAS isoform-specific details of BRAF kinase regulation.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 5 citations in OpenAlex.
- BRAF Inhibition-Associated Nuclear Remodeling is Linked to Cancer-Associated Fibroblast Activation.Cancer research communications · 2026Article
- Longitudinal Live Imaging-Derived 4D Hemodynamics and Dynamic Tissue Mechanics Across Outflow Tract Morphogenesis.Annals of biomedical engineering · 2026Article
- Kinetic Signatures of RAS-BRAF Engagement Reveal Isoform Selectivity, Oncogenic Amplification, and Mutation-Dependent Inhibitor Resistance.bioRxiv : the preprint server for biology · 2026Article
- Divergent CRD-Dependent Mechanisms Govern RAS Isoform-Selective Recruitment of CRAF and ARAF.bioRxiv : the preprint server for biology · 2026Article
- Real-Time Visualization of Isoform-Specific RAF-KRAS Interactions in Living Cells Using FRET-BRET Hybrid Biosensors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Long-term outcomes of cochlear implantation in children with cochlear nerve deficiency: auditory speech performance and predictive factors over 5 years.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026Article
- The BRAF-specific region suppresses cysteine-rich domain-lipid interaction independently of canonical autoinhibition by the 14-3-3 dimer.Protein science : a publication of the Protein Society · 2026Article
- Real time characterization of the MAPK pathway using native mass spectrometry.Communications biology · 2025Article
- Braf-Mutant Melanomas: Biology and Therapy.Current oncology (Toronto, Ont.) · 2024Review
- Activation of NPY2R-expressing amygdala neurons inhibits itch behavior in mice without lateralization.Scientific reports · 2024Article
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
BRAF is a key member in the MAPK signaling pathway essential for cell growth, proliferation, and differentiation. Mutant BRAF is often the underlying cause of various types of cancer and mutant RAS, the upstream regulator of BRAF, is a driver of up to one-third of all cancers. BRAF interacts with RAS and undergoes a conformational change from an inactive, autoinhibited monomer to an active dimer, which propagates downstream signaling. Because of BRAF's complex regulation mechanism, the exact order and magnitude of its activation steps have yet to be confirmed experimentally. By studying the inter- and intramolecular interactions of BRAF, we unveil the domain-specific and isoform-specific details of BRAF regulation through pulldown assays, open surface plasmon resonance (OpenSPR), and hydrogen-deuterium exchange mass spectrometry (HDX-MS). We demonstrate that the BRAF specific region (BSR) and cysteine rich domain (CRD) play a crucial role in regulating the activation of BRAF in a RAS isoform-specific manner. Moreover, we quantified the binding affinities between BRAF N-terminal and kinase domains (KD) to reveal their individual roles in autoinhibition. Our findings also indicate that oncogenic BRAF-KD
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.