Evidence map›Paper›PMID 9418899›Full record

ArticleMolecular and cellular biology1998

Constitutive activation of the aromatic hydrocarbon receptor.

C Y Chang, A Puga

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
16.0field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 243 citations in OpenAlex.

  1. Article
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  9. Developmental Regulation of Nuclear Factor Erythroid-2 Related Factors (nrfs) by AHR1b in Zebrafish (Danio rerio).Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
  10. Regulation of Astrocyte Functions in Multiple Sclerosis.Cold Spring Harbor perspectives in medicine · 2019
    Review
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  14. Review
  15. Genistein PreventsCurrent developments in nutrition · 2017
    Article
  16. Article
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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

2 authors at 1 institution in 1 country.

C Y ChangDepartment of Environmental Health, University of Cincinnati Medical Center, Ohio 45267-0056, USA.
A Puga
University of Cincinnati · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI YADAV, JAGJIT S · 1992 to 2022
$35.4M
MOLECULAR MECHANISMS OF DIOXIN ACTIONR01ES006273 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 1993 to 2015
$4.6M
Molecular Mechanisms of Dioxin ActionR56ES006273 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 2009 to 2009
$454k
NIEHS NIH HHS ES06273NIEHS NIH HHS P30 ES006096NIEHS NIH HHS P30 ES06096NIEHS NIH HHS R01 ES006273NIEHS NIH HHS R56 ES006273
6 · The paper itself

Abstract

The ligand-activated aromatic hydrocarbon receptor (AHR) dimerizes with the AHR nuclear translocator (ARNT) to form a functional complex that transactivates expression of the cytochrome P-450 CYP1A1 gene and other genes in the dioxin-inducible [Ah] gene battery. Previous work from this laboratory has shown that the activity of the CYP1A1 enzyme negatively regulates this process. To study the relationship between CYP1A1 activity and Ah receptor activation we used CYP1A1-deficient mouse hepatoma c37 cells and CYP1A1- and AHR-deficient African green monkey kidney CV-1 cells. Using gel mobility shift and luciferase reporter gene expression assays, we found that c37 cells that had not been exposed to exogenous Ah receptor ligands already contained transcriptionally active AHR-ARNT complexes, a finding that we also observed in wild-type Hepa-1 cells treated with Ellipticine, a CYP1A1 inhibitor. In CV-1 cells, transient expression of AHR and ARNT leads to high levels of AHR-ARNT-dependent luciferase gene expression even in the absence of an agonist. Using a green fluorescent protein-tagged AHR, we showed that elevated reporter gene expression correlates with constitutive nuclear localization of the AHR. Transcriptional activation of the luciferase reporter gene observed in CV-1 cells is significantly decreased by (i) expression of a functional CYP1A1 enzyme, (ii) competition with chimeric or truncated AHR proteins containing the AHR ligand-binding domain, and (iii) treatment with the AHR antagonist alpha-naphthoflavone. These results suggest that a CYP1A1 substrate, which accumulates in cells lacking CYP1A1 enzymatic activity, is an AHR ligand responsible for endogenous activation of the Ah receptor.

Indexed as

Gene Expression RegulationAnimalsCell LineCytochrome P-450 CYP1A1DNA, ComplementaryGene Transfer TechniquesHaplorhiniMiceReceptors, Aryl HydrocarbonCytochrome P-450 CYP1A1DNA, ComplementaryReceptors, Aryl Hydrocarbon

Identifiers

PMID9418899
PMCPMC121520
OpenAlexW2149540498

What OpenQuestion holds

Textmetadata
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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.