Evidence map›Paper›PMID 26412238›Full record

ArticleScientific reports2015

Activating transcription factor 3 represses inflammatory responses by binding to the p65 subunit of NF-κB.

Ji-Woong Kwon, Hyuk-Kwon Kwon, Hyeon-Jun Shin, Yong-Min Choi, Muhammad Ayaz Anwar, Sangdun Choi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

63 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  4. Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026
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  9. Article
  10. Review
  11. The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  12. Article
  13. Article
  14. ST32da, a NovelCells · 2025
    Article
  15. [ATF3 regulates inflammatory response in atherosclerotic plaques in mice through the NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

3 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Ji-Woong KwonDepartment of Molecular Science and Technology, Ajou University, Suwon, 443-749, Korea.
Hyuk-Kwon KwonDepartment of Molecular Science and Technology, Ajou University, Suwon, 443-749, Korea.
Hyeon-Jun ShinDepartment of Molecular Science and Technology, Ajou University, Suwon, 443-749, Korea.
Yong-Min ChoiDepartment of Molecular Science and Technology, Ajou University, Suwon, 443-749, Korea.
Muhammad Ayaz AnwarDepartment of Molecular Science and Technology, Ajou University, Suwon, 443-749, Korea.
Sangdun ChoiDepartment of Molecular Science and Technology, Ajou University, Suwon, 443-749, Korea.
Ajou University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating transcription factor 3 (ATF3) is induced by inflammatory responses, cell death, cytokines, and oxidative stress conditions. ATF3 is a negative regulator in the Toll-like receptor 4 signalling pathway. The principal molecule in this pathway is nuclear factor κB (NF-κB) that translocates into the nucleus to initiate the transcription of inflammatory mediators. However, scarce data are available regarding the interaction of ATF3 and p65, a part of the NF-κB dimer. Therefore, we studied the mechanism of regulation of p65 by ATF3 in RAW 264.7 cells. First, LPS-mediated NF-κB activation was confirmed, and then the direct interaction of ATF3 and p65 was observed through immunoprecipitation (IP). The presence of histone deacetylase 1 (HDAC1) was also detected in the complex. In ATF3 deficient cells, NF-κB activity was up-regulated and HDAC1 was not detected by IP. These observations suggest that p65 is attenuated by ATF3 such that ATF3 recruits HDAC1 to the ATF3/p65 complex and facilitates the deacetylation of p65. Likewise, inflammatory response genes were induced by translocated NF-κB in ATF3-deficient cells. Cumulatively, we uncovered a novel mechanism for the negative regulation of NF-κB by ATF3 via direct interaction with p65.

Indexed as

Activating Transcription Factor 3AnimalsCell LineEnzyme ActivationGene Expression RegulationHistone Deacetylase 1HumansInflammationLipopolysaccharidesMacrophagesMiceProtein BindingProtein TransportSignal TransductionTranscription Factor RelAActivating Transcription Factor 3Histone Deacetylase 1LipopolysaccharidesTranscription Factor RelA

Identifiers

PMID26412238
PMCPMC4585983
OpenAlexW2336328518

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.