Evidence map›Paper›PMID 24386331›Full record

ArticlePloS one2013

Regulation of c-Fos gene expression by NF-κB: a p65 homodimer binding site in mouse embryonic fibroblasts but not human HEK293 cells.

Yu-Cheng Tu, Duen-Yi Huang, Shine-Gwo Shiah, Jang-Shiun Wang, Wan-Wan Lin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.5field-weighted citation impact, top 32% of its field
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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  2. Mouse Trophoblast Stem Cells Are Deficient in TNFα-Activated NFκB Signaling Pathway and Inflammatory Response.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
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  7. Post-stroke brain can be protected by modulating the lncRNA FosDT.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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  15. Antcin-H Isolated fromEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
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  17. 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

5 authors at 2 institutions in 1 country.

Yu-Cheng TuDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Duen-Yi HuangDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shine-Gwo ShiahNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli County, Taiwan.
Jang-Shiun WangDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wan-Wan LinDepartment of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan ; Graduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan.
National Taiwan University · TWNational Health Research Institutes · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immediate early gene c-Fos is reported to be regulated by Elk-1 and cAMP response element-binding protein (CREB), but whether nuclear factor (NF)-κB is also required for controlling c-Fos expression is unclear. In this study, we determined how NF-κB's coordination with Elk/serum response factor (SRF) regulates c-fos transcription. We report that PMA strongly induced c-Fos expression, but tumor necrosis factor (TNF)-α did not. In mouse embryonic fibroblasts, the PMA induction of c-Fos was suppressed by a deficiency in IKKα, IKKβ, IKKγ, or p65. By contrast, in human embryonic kidney 293 cells, PMA induced c-Fos independently of p65. In accordance with these results, we identified an NF-κB binding site in the mouse but not human c-fos promoter. Under PMA stimulation, IKKα/β mediated p65 phosphorylation and the binding of the p65 homodimer to the NF-κB site in the mouse c-fos promoter. Furthermore, our studies demonstrated independent but coordinated functions of the IKKα/β-p65 and extracellular signal-regulated kinase (ERK)-Elk-1 pathways in the PMA induction of c-Fos. Collectively, these results reveal the distinct requirement of NF-κB for mouse and human c-fos regulation. Binding of the p65 homodimer to the κB site was indispensable for mouse c-fos expression, whereas the κB binding site was not present in the human c-fos promoter. Because of an inability to evoke sufficient ERK activation and Elk-1 phosphorylation, TNF-α induces c-Fos more weakly than PMA does in both mouse and human cells.

Indexed as

Gene Expression RegulationProtein MultimerizationAnimalsBase SequenceBinding SitesEnzyme Activationets-Domain Protein Elk-1Extracellular Signal-Regulated MAP KinasesFibroblastsHEK293 CellsHumansI-kappa B KinaseMicePhosphorylationPromoter Regions, GeneticProtein Structure, QuaternaryElk1 protein, mouseets-Domain Protein Elk-1Extracellular Signal-Regulated MAP KinasesI-kappa B KinaseProto-Oncogene Proteins c-fosTetradecanoylphorbol AcetateTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID24386331
PMCPMC3875526
OpenAlexW2046637663

What OpenQuestion holds

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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.