Evidence map›Paper›PMID 26543888›Full record

ArticleData in brief2015

ChIP-Seq analysis of the adult male mouse brain after developmental exposure to arsenic.

Christina R Tyler, Jessica A Weber, Matthew Labrecque, Justin M Hessinger, Jeremy S Edwards, Andrea M Allan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Data in brief, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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  5. Review
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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

6 authors.

Christina R TylerDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Jessica A WeberDepartment of Biology, University of New Mexico, Albuquerque, NM 87131, USA.
Matthew LabrecqueDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Justin M HessingerDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Jeremy S EdwardsDepartment of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, NM 87131, USA ; Department of Chemical & Nuclear Engineering, University of New Mexico, Albuquerque, NM 87131, USA ; Department of Chemistry & Chemical Biology, University of New Mexico, Albuquerque, NM 87131, USA ; Cancer Research & Treatment Center, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Andrea M AllanDepartment of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.

Funding

Prenatal arsenic exposure alters transcriptional, post-transcriptional and post-translational programming of the glucocorticoid system in a sexually dimorphic mannerR01ES019583 · NIEHS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI ALLAN, ANDREA M · 2011 to 2021
$3.3M
NIEHS NIH HHS R01 ES019583
6 · The paper itself

Abstract

Exposure to the common environmental contaminant arsenic impacts the epigenetic landscape, including DNA methylation and histone modifications, of several cell types. Developmental arsenic exposure (DAE) increases acetylation and methylation of histone proteins and the protein expression of several chromatin-modifying enzymes in the dentate gyrus (DG) subregion of the adult male mouse brain [26]. To complement and support these data, ChIP-Seq analysis of DNA associated with trimethylation of histone 3 lysine 4 (H3K4me3) derived from the adult male DG after DAE was performed. DAE induced differential H3K4me3 enrichment on genes in pathways associated with cellular development and growth, cell death and survival, and neurological disorders, particularly as they relate to cancer, in the adult male brain. Comparison of H3K4me3 enrichment in controls revealed mechanisms that are potentially lacking in arsenic-exposed animals, including neurotransmission, neuronal growth and development, hormonal regulation, protein synthesis, and cellular homeostasis. New pathways impacted by arsenic include cytoskeleton organization, cell signaling, and potential disruption of immune function and warrant further investigation using this DAE paradigm in the mouse brain.

Identifiers

PMID26543888
PMCPMC4589800

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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.