Evidence map›Paper›PMID 20819909›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2010

An integrated genomic analysis of aryl hydrocarbon receptor-mediated inhibition of B-cell differentiation.

K Nadira De Abrew, Norbert E Kaminski, Russell S Thomas

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

K Nadira De AbrewThe Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709, USA.
Norbert E Kaminski
Russell S Thomas
The Hamner Institutes for Health Sciences · USMichigan State University · 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
TOXIC EFFECTS OF TCDD ON B CELLSR01ES002520 · NIEHS · VIRGINIA COMMONWEALTH UNIVERSITY · PI KAMINSKI, NORBERT E · 1986 to 2016
$4.2M
NIEHS NIH HHS P42 ES004911NIEHS NIH HHS P42-ES004911NIEHS NIH HHS R01 ES002520NIEHS NIH HHS R01 ES02520
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters differentiation of B cells and suppresses antibody production. A combination of whole-genome, microarray-based chromatin immunoprecipitation (ChIP-on-chip), and time course gene expression microarray analysis was performed on the mouse B-cell line CH12.LX following exposure to lipopolysaccharide (LPS) or LPS and TCDD to identify the primary and downstream transcriptional elements of B-cell differentiation that are altered by the AHR. ChIP-on-chip analysis identified 1893 regions with a significant increase in AHR binding with TCDD treatment. Transcription factor binding site analysis on the ChIP-on-chip data showed enrichment in AHR response elements. Other transcription factors showed significant coenrichment with AHR response elements. When ChIP-on-chip regions were compared with gene expression changes at the early time points, 78 genes were identified as potential direct targets of the AHR. AHR binding and expression changes were confirmed for a subset of genes in primary mouse B cells. Network analysis examining connections between the 78 potential AHR target genes and three transcription factors known to regulate B-cell differentiation indicated multiple paths for potential regulation by the AHR. Enrichment analysis on the differentially expressed genes at each time point evaluated the downstream impact of AHR-regulated gene expression changes on B-cell-related processes. AHR-mediated impairment of B-cell differentiation occurred at multiple nodes of the B-cell differentiation network and potentially through multiple mechanisms including direct cis-acting effects on key regulators of B-cell differentiation, indirect regulation of B-cell differentiation-related pathways, and transcriptional coregulation of target genes by AHR and other transcription factors.

Indexed as

GenomicsAnimalsB-LymphocytesCell DifferentiationCell Line, TumorDrug Therapy, CombinationEnvironmental PollutantsFemaleGene ExpressionGene Expression ProfilingImmunosuppressive AgentsLipopolysaccharidesLymphocyte ActivationMiceMice, Inbred C57BLOligonucleotide Array Sequence AnalysisEnvironmental PollutantsImmunosuppressive AgentsLipopolysaccharidesPolychlorinated DibenzodioxinsReceptors, Aryl Hydrocarbon

Identifiers

PMID20819909
PMCPMC3003543
OpenAlexW2098500847

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.