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

MEK Inhibition Reverses Aberrant Signaling in Melanoma Cells through Reorganization of NRas and BRAF in Self Nanoclusters.

Cancer research - 1 Mar 2021

Yakovian Oren, Sajman Julia, Arafeh Rand, Neve-Oz Yair, Alon Michal, Samuels Yardena, Sherman Eilon

Abstract excerpt

Hotspot mutations of the oncogenes BRAF and NRas are the most common genetic alterations in cutaneous melanoma. Still, the nanoscale organization and signal coupling of these proteins remain incompletely understood, particularly upon expression of oncogenic NRas mutants. Here we employed single-molecule localization microscopy to study the nanoscale organization of NRas and BRAF at the plasma membrane (PM) of...

Read the complete abstract on PubMed

Topics

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

Share to Epidermal Growth Factor
Share to Extracellular Signal-Regulated MAP Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to GTP Phosphohydrolases

Share to MAP Kinase Kinase 1

Share to Melanoma, Cutaneous Malignant

Share to Pyridones

Share to Pyrimidinones

Share to Single Molecule Imaging

Source

Open in PubMed Open full text

Identifiers

PMID: 33355187
DOI: 10.1158/0008-5472.CAN-20-1205
PMCID: PMC7617077

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

MEK Inhibition Reverses Aberrant Signaling in Melanoma Cells through Reorganization of NRas and BRAF in Self Nanoclusters.PMID 33355187Read ↗

NRas Nanoclusters Mediate Crosstalk Between BRAF/ERK and PI3K/AKT Signalling in Melanoma CellsSemantic proximity Read ↗

Blocking Nitrosylation Induces Immunogenic Cell Death by Sensitizing NRAS-Mutant Melanoma to MEK Inhibitors.Semantic proximity Read ↗

Efficient Suppression of NRAS-Driven Melanoma by Co-Inhibition of ERK1/2 and ERK5 MAPK Pathways.Semantic proximity Read ↗

MIG6 Is MEK Regulated and Affects EGF-Induced Migration in Mutant NRAS Melanoma.Semantic proximity Read ↗

A Genome-Wide Screen Identifies PDPK1 as a Target to Enhance the Efficacy of MEK1/2 Inhibitors in NRAS Mutant Melanoma.Semantic proximity Read ↗

Sensitivity of Melanoma Cells to EGFR and FGFR Activation but Not Inhibition is Influenced by Oncogenic BRAF and NRAS Mutations.Semantic proximity Read ↗

ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma.Semantic proximity Read ↗

Targeting NRAS in melanoma.Semantic proximity Read ↗

Mechanism of MEK1 phosphorylation by the N-terminal acidic motif-mediated asymmetric BRAF dimer.Semantic proximity Read ↗

HSP70 inhibition blocks adaptive resistance and synergizes with MEK inhibition for the treatment of NRAS-mutant melanoma.Semantic proximity Read ↗

Targeting TBK1 inhibits migration and resistance to MEK inhibitors in mutant NRAS melanoma.Semantic proximity Read ↗

EGFR transactivates RON to drive oncogenic crosstalk.Semantic proximity Read ↗

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