Evidence map›Paper›PMID 22427656›Full record

ArticleThe Journal of biological chemistry2012

Nuclear factor of activated T cells 1 (NFAT1)-induced permissive chromatin modification facilitates nuclear factor-κB (NF-κB)-mediated interleukin-9 (IL-9) transactivation.

Arijita Jash, Anupama Sahoo, Gi-Cheon Kim, Chang-Suk Chae, Ji-Sun Hwang, Jung-Eun Kim, Sin-Hyeog Im

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

44 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Synergistic roles of NFATc1 and c-Jun in immunomodulation.Biochemistry and biophysics reports · 2025
    Review
  5. Article
  6. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  7. Article
  8. Go to the scene: TJournal for immunotherapy of cancer · 2025
    Article
  9. Review
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  11. Article
  12. Review
  13. Review
  14. The CaPharmaceutics · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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 at 2 institutions in 2 countries.

Arijita JashSchool of Life Sciences and Immune Synapse Research Center, Gwangju Institute of Science and Technology, 123 Cheomdan-gwagiro, Buk-gu, Gwangju 500-712, Korea.
Anupama Sahoo
Gi-Cheon Kim
Chang-Suk Chae
Ji-Sun Hwang
Jung-Eun Kim
Sin-Hyeog Im
Gwangju Institute of Science and Technology · KRThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-9 regulates diverse inflammatory immune responses. Although the functional importance of IL-9 has been investigated in various pathophysiological conditions, molecular mechanisms by which TCR stimulation induced IL-9 gene expression are still unclear. In this study, we investigated the functional importance of the NFAT1 and NF-κB (p65) in IL-9 gene transcription in CD4(+) T cells. In vivo binding of NFAT1 and NF-κB (p65) to the IL-9 promoter was observed. NFAT1 binding induced a transcriptionally active chromatin configuration at the IL-9 promoter locus, whereas NF-κB (p65) binding transactivated the IL-9 promoter. Mouse deficient in NFAT1 shows a significant down-regulation of IL-9 expression that resulted from an inaccessible chromatin configuration at the IL-9 promoter. In parallel, knockdown of NF-κB (p65) also resulted in reduced IL-9 expression. In this process, NFAT1 plays a pivotal role as a core protein that creates an accessible platform for the assembly of transcription activators. The presence of NFAT1 correlates with recruitment of NF-κB (p65), p300, and active histone markers on the IL-9 promoter, resulting in a transcriptionally competent promoter. NFAT1 deficiency significantly reduced the recruitment of the above activation complex to the IL-9 promoter. In summary, our data suggest that functional cooperation of NFAT1 and NF-κB synergistically enhances IL-9 transcription in CD4(+) T cells.

Indexed as

Transcriptional ActivationAnimalsBase SequenceBinding SitesCD4-Positive T-LymphocytesCells, CulturedChromatinChromatin ImmunoprecipitationHEK293 CellsHumansImmunoblottingInterleukin-9MiceMice, Inbred C57BLMice, KnockoutMolecular Sequence DataChromatinInterleukin-9NFATC Transcription FactorsTranscription Factor RelA

Identifiers

PMID22427656
PMCPMC3346086
OpenAlexW1987528629

What OpenQuestion holds

Textmetadata
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.