Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

BRAF Splice Variant Resistance to RAF Inhibitor Requires Enhanced MEK Association

1 Nov 2018

Abstract excerpt

Expression of aberrantly spliced BRAF V600E isoforms (BRAF V600E ΔEx) mediates resistance in 13%-30% of melanoma patients progressing on RAF inhibitors. BRAF V600E ΔEx confers resistance, in part, through enhanced dimerization. Here, we uncoupled BRAF V600E ΔEx dimerization from maintenance of MEK-ERK1/2 signaling. Furthermore, we show BRAF V600E ΔEx association with its substrate, MEK, is enhanced and required...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cytokine Signaling Pathways and Interactions
Share to Melanoma and MAPK Pathways
Share to Protein Kinase Regulation and GTPase Signaling

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 30404005
DOI: 10.1016/j.celrep.2018.10.049

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

BRAF Splice Variant Resistance to RAF Inhibitor Requires Enhanced MEK AssociationPMID 30404005Read ↗

BRAF Mutants Evade ERK-Dependent Feedback by Different Mechanisms that Determine Their Sensitivity to Pharmacologic Inhibition.Semantic proximity Read ↗

Role of serine 365 in BRAF V600E sensitivity to RAF inhibition.Semantic proximity Read ↗

Inhibition of mutant <scp>BRAF</scp> splice variant signaling by next‐generation, selective <scp>RAF</scp> inhibitorsSemantic proximity Read ↗

Identification and Characterization of a B-Raf Kinase α-Helix Critical for the Activity of MEK Kinase in MAPK Signaling.Semantic proximity Read ↗

Melanomagenesis driven by a kinase-dead mutant BRAF lacking codons 600-618Semantic proximity Read ↗

Tumorigenesis driven by the BRAF <sup>V600E</sup> oncoprotein requires secondary mutations that overcome its feedback inhibition of migration and invasionSemantic proximity Read ↗

A Secondary Mutation in BRAF Confers Resistance to RAF Inhibition in a BRAFV600E-Mutant Brain Tumor.Semantic proximity Read ↗

Beneficial Effects of RAF Inhibitor in Mutant BRAF Splice Variant–Expressing MelanomaSemantic proximity Read ↗

BRAF oncogenic mutants evade autoinhibition through a common mechanism.Semantic proximity Read ↗

Paradoxical activation and RAF inhibitor resistance of BRAF protein kinase fusions characterizing pediatric astrocytomas.Semantic proximity Read ↗

BRAF(V600E) Kinase Domain Duplication Identified in Therapy-Refractory Melanoma Patient-Derived Xenografts.Semantic proximity Read ↗

Off-targets of BRAF inhibitors disrupt endothelial signaling and vascular barrier function.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.