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

KappaB-Ras is a nuclear-cytoplasmic small GTPase that inhibits NF-kappaB activation through the suppression of transcriptional activation of p65/RelA.

The Journal of biological chemistry - 1 Oct 2010

Tago Kenji, Funakoshi-Tago Megumi, Sakinawa Masaki, Mizuno Norikazu, Itoh Hiroshi

Abstract excerpt

NF-κB is an important transcription factor involved in various biological responses, including inflammation, cell differentiation, and tumorigenesis. κB-Ras was identified as an IκB-interacting small GTPase and is reported to disturb cytokine-induced NF-κB activation. In this study, we established that κB-Ras is a novel type of nuclear-cytoplasmic small GTPase that mainly binds to GTP, and its localization seemed...

Read the complete abstract on PubMed

Topics

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

Share to Cell Nucleus
Share to Cytoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Guanosine Diphosphate

Share to Guanosine Triphosphate

Share to Monomeric GTP-Binding Proteins

Share to NIH 3T3 Cells

Share to Transcription Factor RelA

Share to Transcriptional Activation

Source

Open in PubMed Open full text

Identifiers

PMID: 20639196
DOI: 10.1074/jbc.M110.117028
PMCID: PMC2945557

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

KappaB-Ras is a nuclear-cytoplasmic small GTPase that inhibits NF-kappaB activation through the suppression of transcriptional activation of p65/RelA.PMID 20639196Read ↗

κB-Ras Proteins Regulate Both NF-κB-Dependent Inflammation and Ral-Dependent ProliferationSemantic proximity Read ↗

κB-Ras proteins are fast-exchanging GTPases and function via nucleotide-independent binding of Ral GTPase-activating protein complexes.Semantic proximity Read ↗

NF‐κB signaling in inflammation and cancerSemantic proximity Read ↗

The Nuclear NF-κB Regulator IκBζ: Updates on Its Molecular Functions and Pathophysiological RolesSemantic proximity Read ↗

IkappaBalpha and IkappaBalpha /NF-kappa B complexes are retained in the cytoplasm through interaction with a novel partner, RasGAP SH3-binding protein 2.Semantic proximity Read ↗

Control of transforming growth factor β signal transduction by small GTPasesSemantic proximity Read ↗

Requirement of the NF-κB Subunit p65/RelA for K-Ras–Induced Lung TumorigenesisSemantic proximity Read ↗

Requirement of NF-κB Activation to Suppress p53-Independent Apoptosis Induced by Oncogenic RasSemantic proximity Read ↗

The B cell antigen receptor controls AP-1 and NFAT activity through Ras-mediated activation of Ral.Semantic proximity Read ↗

Involvement of DNA binding domain in the cellular stability and importin affinity of NF-κB component RelB.Semantic proximity Read ↗

Analysis of the RelA:CBP/p300 Interaction Reveals Its Involvement in NF-κB-Driven TranscriptionSemantic proximity Read ↗

The central role of nuclear factor-κB in mesangial cell activationSemantic proximity Read ↗

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