Evidence map›Paper›PMID 21616089›Full record

ArticleToxicology and applied pharmacology2011

The aryl hydrocarbon receptor interacts with ATP5α1, a subunit of the ATP synthase complex, and modulates mitochondrial function.

Dorothy M Tappenden, Scott G Lynn, Robert B Crawford, KangAe Lee, Ajith Vengellur, Norbert E Kaminski, Russell S Thomas, John J LaPres

Abstract readComparative Study
In one paragraph

Article in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. AhR activation inhibits DRP1-induced mitochondrial fission in airway smooth muscle during asthma.American journal of respiratory cell and molecular biology · 2026
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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

8 authors at 2 institutions in 1 country.

Dorothy M TappendenDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824-1319, USA.
Scott G Lynn
Robert B Crawford
KangAe Lee
Ajith Vengellur
Norbert E Kaminski
Russell S Thomas
John J LaPres
Michigan State University · USThe Hamner Institutes for Health Sciences · US

Funding

VOLATILE ORGANIC CONTAMINANTS--QUANTIFYING THEIR MOVEMENT IN THE UNSATURATED ZONEP42ES004911 · NIEHS · MICHIGAN STATE UNIVERSITY · PI Timothy R. Zacharewski · 1989 to 2026
$64.9M
NIEHS NIH HHS P42 ES004911NIEHS NIH HHS P42 ES04911
6 · The paper itself

Abstract

Dioxins, including 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), produce a wide range of toxic effects in mammals. Most, if not all, of these toxic effects are regulated by the aryl hydrocarbon receptor (AHR). The AHR is a ligand activated transcription factor that has been shown to interact with numerous proteins capable of influencing the receptor's function. The ability of secondary proteins to alter AHR-mediated transcriptional events, a necessary step for toxicity, led us to determine whether additional interacting proteins could be identified. To this end, we have employed tandem affinity purification (TAP) of the AHR in Hepa1c1c7 cells. TAP of the AHR, followed by mass spectrometry (MS) identified ATP5α1, a subunit of the ATP synthase complex, as a strong AHR interactor in the absence of ligand. The interaction was lost upon exposure to TCDD. The association was confirmed by co-immunoprecipitation in multiple cell lines. In addition, cell fractionation experiments showed that a fraction of the AHR is found in the mitochondria. To ascribe a potential functional role to the AHR:ATP5α1 interaction, TCDD was shown to induce a hyperpolarization of the mitochondrial membrane in an AHR-dependent and transcription-independent manner. These results suggest that a fraction of the total cellular AHR pool is localized to the mitochondria and contributes to the organelle's homeostasis.

Indexed as

Amino Acid SequenceAnimalsATP Synthetase ComplexesCell LineCell Line, TumorHomeostasisMiceMice, KnockoutMitochondriaMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesMolecular Sequence DataOxidative Phosphorylation Coupling FactorsPolychlorinated DibenzodioxinsProtein BindingProtein SubunitsATP Synthetase ComplexesF(6) ATPaseMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesOxidative Phosphorylation Coupling FactorsPolychlorinated DibenzodioxinsProtein SubunitsReceptors, Aryl Hydrocarbon

Identifiers

PMID21616089
PMCPMC3133825
OpenAlexW2125660831

What OpenQuestion holds

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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.