Evidence map›Paper›PMID 19465110›Full record

ArticleReproductive toxicology (Elmsford, N.Y.)2009

AhR-mediated gene expression in the developing mouse telencephalon.

Julia M Gohlke, Pat S Stockton, Stella Sieber, Julie Foley, Christopher J Portier

Abstract read
In one paragraph

Article in Reproductive toxicology (Elmsford, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Role of environmental pollutants in Alzheimer's disease: a review.Environmental science and pollution research international · 2020
    Review
  8. The Aryl Hydrocarbon Receptor and the Nervous System.International journal of molecular sciences · 2018
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Perspectives on the potential involvement of the AH receptor-dioxin axis in cardiovascular disease.Toxicological sciences : an official journal of the Society of Toxicology · 2011
    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

5 authors at 2 institutions in 1 country.

Julia M GohlkeEnvironmental Systems Biology Group, Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, RTP, NC 27709, USA.
Pat S Stockton
Stella Sieber
Julie Foley
Christopher J Portier
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

CMPB Central Pathology SupportZIGES102505 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SILLS, ROBERT · 2010 to 2013
$35.4M
Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Statistical Models In Toxicology And BiochemistryZIAES048002 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PORTIER, CHRISTOPHER J · 2009 to 2010
$2.9M
STATISTICAL MODELS IN TOXICOLOGY AND BIOCHEMISTRYZ01ES048002 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PORTIER, CHRISTOPHER J · 1988 to 2008
$2.8M
Intramural NIH HHS Z01 ES048002
6 · The paper itself

Abstract

We hypothesize that TCDD-induced developmental neurotoxicity is modulated through an AhR-dependent interaction with key regulatory neuronal differentiation pathways during telencephalon development. To test this hypothesis we examined global gene expression in both dorsal and ventral telencephalon tissues in E13.5 AhR-/- and wildtype mice exposed to TCDD or vehicle. Consistent with previous biochemical, pathological and behavioral studies, our results suggest TCDD initiated changes in gene expression in the developing telencephalon are primarily AhR-dependent, as no statistically significant gene expression changes are evident after TCDD exposure in AhR-/- mice. Based on a gene regulatory network for neuronal specification in the developing telencephalon, the present analysis suggests differentiation of GABAergic neurons in the ventral telencephalon is compromised in TCDD exposed and AhR-/- mice. In addition, our analysis suggests Sox11 may be directly regulated by AhR based on gene expression and comparative genomics analyses. In conclusion, this analysis supports the hypothesis that AhR has a specific role in the normal development of the telencephalon and provides a mechanistic framework for neurodevelopmental toxicity of chemicals that perturb AhR signaling.

Indexed as

AnimalsCell DifferentiationComparative Genomic HybridizationFemaleGene Expression Regulation, DevelopmentalMaleMaternal ExposureMiceMice, Inbred C57BLMice, KnockoutOligonucleotide Array Sequence AnalysisPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRNA, MessengerSignal TransductionSOXC Transcription FactorsPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRNA, MessengerSox11 protein, mouseSOXC Transcription FactorsTeratogens

Identifiers

PMID19465110
PMCPMC2766425
OpenAlexW2092276670

What OpenQuestion holds

Textmetadata
LicenceTDM
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.