Evidence map›Paper›PMID 42390017›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2026

The Nuclear Export Signal of IκBα Drives RelB Oscillations in the Noncanonical NF-κB Pathway.

Takao Seki, Shelly Davis, Shigeki Miyamoto, Taishin Akiyama, Hiroyasu Nakano, Jun-Ichiro Inoue, Katsuhide Okunishi

Abstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. The Nuclear Export Signal of IκBα Drives RelB Oscillations in the Noncanonical NF-κB Pathway.Genes to cells : devoted to molecular & cellular mechanisms · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Takao SekiDivision of Cellular and Molecular Biology, Department of Cancer Biology, The Institute of Medical Science, the University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0003-0202-8632
Shelly DavisDepartment of Oncology, University of Wisconsin Carbone Cancer Center, University of Wisconsin, Madison, Wisconsin, USA.
Shigeki MiyamotoDepartment of Oncology, University of Wisconsin Carbone Cancer Center, University of Wisconsin, Madison, Wisconsin, USA.
Taishin AkiyamaLaboratory for Immune Homeostasis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Hiroyasu NakanoUnit of Host Defense, Faculty of Medicine, Toho University, Tokyo, Japan.
Jun-Ichiro InoueDivision of Cellular and Molecular Biology, Department of Cancer Biology, The Institute of Medical Science, the University of Tokyo, Tokyo, Japan.
Katsuhide OkunishiDepartment of Biochemistry, Faculty of Medicine, Toho University, Tokyo, Japan.

Funding

Impact of Host NF-kB Signaling in Radiation TherapyR01CA246321 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI MIYAMOTO, SHIGEKI · 2021 to 2025
$1.8M
Japan Society for the Promotion of Science 1005679Japan Society for the Promotion of Science 16H06575Japan Society for the Promotion of Science 18390409Japan Society for the Promotion of Science 20390393Japan Society for the Promotion of Science 20K16151Japan Society for the Promotion of Science 22117002Japan Society for the Promotion of Science 26290036Japan Society for the Promotion of Science 925190NCI NIH HHS R01 CA246321NIH HHS R01CA246321
6 · The paper itself

Abstract

The noncanonical NF-κB pathway regulates immune development and inflammation through RelB nuclear translocation, yet the dynamics of this process at the single-cell level remain poorly understood. Using live-cell imaging of RelB-Venus knock-in mouse embryonic fibroblasts, we show that LTβR or TWEAK stimulation induces four distinct RelB nuclear translocation patterns: oscillating, prolonged activation, transient activation, and non-responding. Approximately 40% of cells exhibited oscillatory behavior with a predominant period of 1.5-2.0 h, similar to RelA oscillations in the canonical pathway. Mechanistically, RelB oscillations required CRM1-mediated nuclear export, ongoing protein synthesis, NIK-dependent noncanonical signaling, and the IκBα nuclear export signal. Knockdown or knockout of Nfkb2 (encoding p100) induced spontaneous RelB oscillations without stimulation, identifying p100 as a threshold regulator that controls oscillation probability through cytoplasmic sequestration of RelB. Co-immunoprecipitation analysis revealed dynamic RelB-IκBα complex formation in both cytoplasmic and nuclear fractions following LTβR stimulation. Furthermore, disruption of RelB oscillations in Nfkbia

Indexed as

NF-kappa BNF-KappaB Inhibitor alphaNuclear Export SignalsTranscription Factor RelBActive Transport, Cell NucleusAnimalsCell NucleusExportin 1 ProteinFibroblastsKaryopherinsLymphotoxin beta ReceptorMiceNF-kappa B p52 SubunitReceptors, Cytoplasmic and NuclearSignal TransductionExportin 1 ProteinKaryopherinsLymphotoxin beta ReceptorNF-kappa BNF-KappaB Inhibitor alphaNF-kappa B p52 SubunitNuclear Export SignalsReceptors, Cytoplasmic and NuclearRelb protein, mouseTranscription Factor RelB

Identifiers

PMID42390017
PMCPMC13325521

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.