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

KRASQ61H Preferentially Signals through MAPK in a RAF Dimer-Dependent Manner in Non-Small Cell Lung Cancer.

Cancer research - 1 Sept 2020

Zhou Zhi-Wei, Ambrogio Chiara, Bera Asim K, Li Qing, Li Xing-Xiao, Li Lianbo, Son Jieun, Gondi Sudershan, Li Jiaqi, Campbell Emily, Jin Hua, Okoro Jeffrey J, Xu Cheng-Xiong, Janne Pasi A, Westover Kenneth D

Abstract excerpt

Assembly of RAS molecules into complexes at the cell membrane is critical for RAS signaling. We previously showed that oncogenic KRAS codon 61 mutations increase its affinity for RAF, raising the possibility that KRASQ61H, the most common KRAS mutation at codon 61, upregulates RAS signaling through mechanisms at the level of RAS assemblies. We show here that KRASQ61H exhibits preferential binding to RAF relative...

Read the complete abstract on PubMed

Topics

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

Share to Carcinoma, Non-Small-Cell Lung
Share to HEK293 Cells

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Heterografts

Share to Lung Neoplasms

Share to MAP Kinase Signaling System

Share to Proto-Oncogene Proteins p21(ras)

Share to raf Kinases

Source

Identifiers

PMID: 32605999
DOI: 10.1158/0008-5472.CAN-20-0448

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

KRASQ61H Preferentially Signals through MAPK in a RAF Dimer-Dependent Manner in Non-Small Cell Lung Cancer.PMID 32605999Read ↗

Functional and biological heterogeneity of KRASQ61 mutations.Semantic proximity Read ↗

Targeting the MAPK Pathway in RAS Mutant Cancers.Semantic proximity Read ↗

Structural and functional analyses of a germline KRAS T50I mutation provide insights into Raf activation.Semantic proximity Read ↗

Biochemical and Structural Analysis of Common Cancer-Associated KRAS Mutations.Semantic proximity Read ↗

KRAS insertion mutations are oncogenic and exhibit distinct functional properties.Semantic proximity Read ↗

Nanoclustering and signaling of KRAS G12C and KRAS G12D respond to lipid acyl chain remodeling in an allele-specific mannerSemantic proximity Read ↗

KRAS G12C and KRAS G12D respond to lipid metabolism in an allele-specific manner.Semantic proximity Read ↗

A cancer-associated K-RAS mutant that preferentially binds GDP displays gain-of-function and atypical signalingSemantic proximity Read ↗

Structure of SHOC2-KRAS-PP1C complex reveals RAS isoform-specific determinants and insights into targeting complex assembly by RAS inhibitors.Semantic proximity Read ↗

Dimerization Is Critical for the Functions of Wild-type and Mutant KRAS.Semantic proximity Read ↗

Blocking EGFR palmitoylation suppresses PI3K signaling and mutant KRAS lung tumorigenesisSemantic proximity Read ↗

Structural insights into isoform-specific RAS-PI3Kα interactions and the role of RAS in PI3Kα activationSemantic proximity Read ↗

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