Evidence map›Paper›PMID 19333233›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2009

Ah receptor represses acute-phase response gene expression without binding to its cognate response element.

Rushang D Patel, Iain A Murray, Colin A Flaveny, Ann Kusnadi, Gary H Perdew

Open access · greenAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. The aryl hydrocarbon receptor in liver inflammation.Seminars in immunopathology · 2021
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Multigenerational and Transgenerational Effects of Dioxins.International journal of molecular sciences · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. Article

1 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

5 authors at 1 institution in 1 country.

Rushang D PatelDepartment of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA.
Iain A Murray
Colin A Flaveny
Ann Kusnadi
Gary H Perdew
Pennsylvania State University · US

Funding

REGULATION OF THE AH RECEPTORR01ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H. · 1994 to 2017
$5.3M
BIOCHEMICAL CHARACTERIZATION OF THE AH RECEPTORR29ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H · 1989 to 1993
–
NIEHS NIH HHS ES04869NIEHS NIH HHS R01 ES004869
6 · The paper itself

Abstract

Repression of the nuclear factor-kappaB (NF-kappaB) pathway has been extensively researched because of its pivotal role in inflammation. We investigated the potential of the aryl hydrocarbon receptor (AHR) to suppress NF-kappaB regulated-gene expression, especially acute-phase genes, such as serum amyloid A (Saa). Using AHR mutants, it was determined that nuclear translocation and heterodimerization with AHR-nuclear translocator are essential, but DNA binding is not involved in AHR-mediated Saa repression. A number of AHR ligands were capable of repressing Saa3 expression. AHR activation leads to a decrease in RELA and C/EBP/beta recruitment to and histone acetylation at Saa3 gene promoter. A battery of acute-phase genes (eg C-reactive protein and haptoglobin) induced by cytokine exposure was repressed by AHR activation in mouse hepatocytes. Dietary exposure to an AHR ligand represses cytokine-induced acute-phase response in the liver. Use of a human liver-derived cell line revealed similar repression of Saa mRNA levels and secreted protein. Repression of AHR expression also enhanced Saa induction in response to cytokines, suggesting that AHR is capable of constitutively repressing Saa gene expression. These results establish a role for AHR in inflammatory signaling within the liver, presenting a new therapeutic opportunity, and signify AHR's ability to function in a DNA-independent manner.

Indexed as

Response ElementsAcetylationActive Transport, Cell NucleusAcute-Phase ReactionAnimalsAryl Hydrocarbon Receptor Nuclear TranslocatorCell LineCell NucleusCytokinesFemaleGene Expression RegulationHepatocytesHumansLigandsMiceMice, Inbred C57BLAryl Hydrocarbon Receptor Nuclear TranslocatorCytokinesLigandsNF-kappa BReceptors, Aryl HydrocarbonSAA3P protein, humanSerum Amyloid A Protein

Identifiers

PMID19333233
PMCPMC2743259
OpenAlexW2084800620

What OpenQuestion holds

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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.