Evidence map›Paper›PMID 27060138›Full record

ArticleNucleic acids research2016

Physiological TLR5 expression in the intestine is regulated by differential DNA binding of Sp1/Sp3 through simultaneous Sp1 dephosphorylation and Sp3 phosphorylation by two different PKC isoforms.

Bhupesh Kumar Thakur, Nirmalya Dasgupta, Atri Ta, Santasabuj Das

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Role of post-translational modifications of Sp1 in cancer: state of the art.Frontiers in cell and developmental biology · 2024
    Review
  5. Review
  6. Review
  7. Nutrients · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Toll-Like Receptor 5 of Golden PompanoInternational journal of molecular sciences · 2020
    Article
  12. Article
  13. Epigenetic regulation of Toll-like receptors and its roles in type 1 diabetes.Journal of molecular medicine (Berlin, Germany) · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

4 authors at 1 institution in 1 country.

Bhupesh Kumar ThakurDivision of Clinical Medicine, National Institute of Cholera and Enteric Diseases, P-33, CIT Road, Scheme XM, Beliaghata, Kolkata 700010, India.
Nirmalya DasguptaDivision of Clinical Medicine, National Institute of Cholera and Enteric Diseases, P-33, CIT Road, Scheme XM, Beliaghata, Kolkata 700010, India.
Atri TaDivision of Clinical Medicine, National Institute of Cholera and Enteric Diseases, P-33, CIT Road, Scheme XM, Beliaghata, Kolkata 700010, India.
Santasabuj DasDivision of Clinical Medicine, National Institute of Cholera and Enteric Diseases, P-33, CIT Road, Scheme XM, Beliaghata, Kolkata 700010, India dasss@icmr.org.in.
National Institute of Cholera and Enteric Diseases · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor 5 (TLR5) expression in the intestinal epithelial cells (IECs) is critical to maintain health, as underscored by multiple intestinal and extra-intestinal diseases in mice genetically engineered for IEC-specific TLR5 knockout. A gradient of expression exists in the colonic epithelial cells from the cecum to the distal colon. Intriguingly, an identical gradient for the dietary metabolite, butyrate also exists in the luminal contents. However, both being critical for intestinal homeostasis and immune response, no studies examined the role of butyrate in the regulation of TLR5 expression. We showed that butyrate transcriptionally upregulates TLR5 in the IECs and augments flagellin-induced immune responses. Both basal and butyrate-induced transcription is regulated by differential binding of Sp-family transcription factors to the GC-box sequences over the TLR5 promoter. Butyrate activates two different protein kinase C isoforms to dephosphorylate/acetylate Sp1 by serine/threonine phosphatases and phosphorylate Sp3 by ERK-MAPK, respectively. This resulted in Sp1 displacement from the promoter and binding of Sp3 to it, leading to p300 recruitment and histone acetylation, activating transcription. This is the first study addressing the mechanisms of physiological TLR5 expression in the intestine. Additionally, a novel insight is gained into Sp1/Sp3-mediated gene regulation that may apply to other genes.

Indexed as

AcetylationAnimalsButyratesExtracellular Signal-Regulated MAP KinasesFlagellinGene Expression RegulationHistonesHumansImmunity, CellularIntestinal MucosaMiceMice, Knockoutp300-CBP-Associated Factorp300-CBP Transcription FactorsPromoter Regions, GeneticProtein BindingButyratesExtracellular Signal-Regulated MAP KinasesFlagellinHistonesp300-CBP-Associated Factorp300-CBP Transcription FactorsSp3 protein, mouseSp3 Transcription FactorSp Transcription FactorsToll-Like Receptor 5

Identifiers

PMID27060138
PMCPMC4937308
OpenAlexW2329862917

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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.