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

Oncogenic and RASopathy-associated K-RAS mutations relieve membrane-dependent occlusion of the effector-binding site.

Proceedings of the National Academy of Sciences of the United States of America - 26 May 2015

Mazhab-Jafari Mohammad T, Marshall Christopher B, Smith Matthew J, Gasmi-Seabrook Geneviève M C, Stathopulos Peter B, Inagaki Fuyuhiko, Kay Lewis E, Neel Benjamin G, Ikura Mitsuhiko

Abstract excerpt

K-RAS4B (Kirsten rat sarcoma viral oncogene homolog 4B) is a prenylated, membrane-associated GTPase protein that is a critical switch for the propagation of growth factor signaling pathways to diverse effector proteins, including rapidly accelerated fibrosarcoma (RAF) kinases and RAS-related protein guanine nucleotide dissociation stimulator (RALGDS) proteins. Gain-of-function KRAS mutations occur frequently in...

Read the complete abstract on PubMed

Topics

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

Share to Genes, ras
Share to Lipid Bilayers

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Molecular Dynamics Simulation

Share to Nuclear Magnetic Resonance, Biomolecular

Share to Protein Conformation

Share to Protein Interaction Domains and Motifs

Share to Proto-Oncogene Proteins p21(ras)

Share to Static Electricity

Source

Open in PubMed Open full text

Identifiers

PMID: 25941399
DOI: 10.1073/pnas.1419895112
PMCID: PMC4450377

Genes

ARAF
KRAS
RALGDS

Variants

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

Oncogenic and RASopathy-associated K-RAS mutations relieve membrane-dependent occlusion of the effector-binding site.PMID 25941399Read ↗

GTP Binding and Oncogenic Mutations May Attenuate Hypervariable Region (HVR)-Catalytic Domain Interactions in Small GTPase K-Ras4B, Exposing the Effector Binding Site.Semantic proximity Read ↗

The disordered hypervariable region and the folded catalytic domain of oncogenic K-Ras4B partner in phospholipid binding.Semantic proximity Read ↗

NMR in integrated biophysical drug discovery for RAS: past, present, and future.Semantic proximity Read ↗

Conformational Dynamics Allows Sampling of an "Active-like" State by Oncogenic K-Ras-GDP.Semantic proximity Read ↗

Long-lasting Salt Bridges Provide the Anchoring Mechanism of Oncogenic Kirsten Rat Sarcoma Proteins at Cell Membranes.Semantic proximity Read ↗

The plasma membrane as a competitive inhibitor and positive allosteric modulator of KRas4B signalingSemantic proximity Read ↗

K-Ras G-domain binding with signaling lipid phosphoinositides: PIP2 association, orientation, functionSemantic proximity Read ↗

NMR-based functional profiling of RASopathies and oncogenic RAS mutationsSemantic proximity Read ↗

The Structural Basis of Oncogenic Mutations G12, G13 and Q61 in Small GTPase K-Ras4B.Semantic proximity Read ↗

Small-molecule modulation of Ras signaling.Semantic proximity Read ↗

Arl2-Mediated Allosteric Release of Farnesylated KRas4B from Shuttling Factor PDEδ.Semantic proximity Read ↗

Drugging Ras GTPase: a comprehensive mechanistic and signaling structural view.Semantic proximity Read ↗

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