Evidence map›Paper›PMID 18524851›Full record

ArticleMolecular biology of the cell2008

The aryl hydrocarbon receptor binds to E2F1 and inhibits E2F1-induced apoptosis.

Jennifer L Marlowe, Yunxia Fan, Xiaoqing Chang, Li Peng, Erik S Knudsen, Ying Xia, Alvaro Puga

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2008. 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
6.2field-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

57 citing papers in PubMed, 129 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The Role of Aryl Hydrocarbon Receptor in Bone Biology.International journal of tryptophan research : IJTR · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Metabolites ofFood science of animal resources · 2022
    Article
  13. Review
  14. Review
  15. The Landscape of AhR Regulators and Coregulators to Fine-Tune AhR Functions.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Review
  18. The Aryl Hydrocarbon Receptor and the Maintenance of Lung Health.International journal of molecular sciences · 2018
    Review
  19. Role of Sequence Variations inCurrent genomics · 2018
    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 1 country.

Jennifer L MarloweDepartment of Environmental Health and Center for Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0056, USA.
Yunxia Fan
Xiaoqing Chang
Li Peng
Erik S Knudsen
Ying Xia
Alvaro Puga
University of Cincinnati Medical Center · USUniversity 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 COMPLEX MIXTURE TOXICITYR01ES010807 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 2001 to 2021
$8.0M
MOLECULAR MECHANISMS OF DIOXIN ACTIONR01ES006273 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 1993 to 2015
$4.6M
NIEHS NIH HHS P30 ES006096NIEHS NIH HHS P30 ES-06096NIEHS NIH HHS R01 ES006273NIEHS NIH HHS R01 ES010807NIEHS NIH HHS R01 ES-06273NIEHS NIH HHS R01 ES-10807
6 · The paper itself

Abstract

Cellular stress by DNA damage induces checkpoint kinase-2 (CHK2)-mediated phosphorylation and stabilization of the E2F1 transcription factor, leading to induction of apoptosis by activation of a subset of proapoptotic E2F1 target genes, including Apaf1 and p73. This report characterizes an interaction between the aryl hydrocarbon (Ah) receptor (AHR), a ligand-activated transcription factor, and E2F1 that results in the attenuation of E2F1-mediated apoptosis. In Ahr(-/-) fibroblasts stably transfected with a doxycycline-regulated AHR expression vector, inhibition of AHR expression causes a significant elevation of oxidative stress, gammaH2A.X histone phosphorylation, and E2F1-dependent apoptosis, which can be blocked by small interfering RNA-mediated knockdown of E2F1 expression. In contrast, ligand-dependent AHR activation protects these cells from etoposide-induced cell death. In cells expressing both proteins, AHR and E2F1 interact independently of the retinoblastoma protein (RB), because AHR and E2F1 coimmunoprecipitate from extracts of RB-negative cells. Additionally, chromatin immunoprecipitation assays indicate that AHR and E2F1 bind to the Apaf1 promoter at a region containing a consensus E2F1 binding site but no AHR binding sites. AHR activation represses Apaf1 and TAp73 mRNA induction by a constitutively active CHK2 expression vector. Furthermore, AHR overexpression blocks the transcriptional induction of Apaf1 and p73 and the accumulation of sub-G(0)/G(1) cells resulting from ectopic overexpression of E2F1. These results point to a proproliferative, antiapoptotic function of the Ah receptor that likely plays a role in tumor progression.

Indexed as

ApoptosisOxidative StressAnimalsApoptotic Protease-Activating Factor 1Cell CycleCell Line, TumorE2F1 Transcription FactorFibroblastsHistonesHumansMiceModels, BiologicalPromoter Regions, GeneticReceptors, Aryl HydrocarbonAPAF1 protein, humanApaf1 protein, mouseApoptotic Protease-Activating Factor 1E2F1 Transcription FactorHistonesReceptors, Aryl Hydrocarbon

Identifiers

PMID18524851
PMCPMC2488290
OpenAlexW2104456356

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.