Evidence map›Paper›PMID 24495120›Full record

ReviewAnnals of the New York Academy of Sciences2014

The Ah receptor in stem cell cycling, regulation, and quiescence.

Thomas A Gasiewicz, Kameshwar P Singh, J Allen Bennett

Open access · bronzeAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 81 citations in OpenAlex.

  1. Aryl hydrocarbon receptor activation alters emergency hematopoiesis during influenza A virus infection.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  2. Review
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  5. The Aryl Hydrocarbon Receptor, Epigenetics and the Aging Process.The journal of nutrition, health & aging · 2023
    Article
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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 1 institution in 1 country.

Thomas A GasiewiczDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, New York.
Kameshwar P Singh
J Allen Bennett
University of Rochester Medical Center · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
TCDD EFFECT ON T LYMPHOCYTE DIFFERENTIATIONR01ES004862 · NIEHS · UNIVERSITY OF ROCHESTER · PI LAWRENCE, B PAIGE · 1990 to 2020
$6.5M
A Role of the Ah Receptor in Hematopoiesis: Model CharacterizationR03ES016606 · NIEHS · UNIVERSITY OF ROCHESTER · PI GASIEWICZ, THOMAS A · 2009 to 2010
$153k
NIEHS NIH HHS ES01247NIEHS NIH HHS ES016606NIEHS NIH HHS ES04862NIEHS NIH HHS ES07026NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES004862NIEHS NIH HHS R03 ES016606NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

Processes that regulate quiescence, self-renewal, and differentiation of hematopoietic stem cells (HSCs) are not well understood. Owing, in part, to the ability of xenobiotic ligands to have persistent effects on the immune system in experimental animals, there has been much work to define a physiological role of the aryl hydrocarbon receptor (AhR) and its relationship to human disease. Persistent AhR activation by dioxin, a potent agonist, results in altered numbers and function of HSCs in mice. HSCs from AhR(-/-) knockout (KO) mice are hyperproliferative and have an altered cell cycle. Aging KO mice show characteristics consistent with premature bone marrow exhaustion. We propose that the increased proliferation of HSCs lacking AhR expression or activity is a result of loss of quiescence, and as such, AhR normally acts as a negative regulator to curb excessive or unnecessary proliferation. Similarly, prolonged and/or inappropriate stimulation of AhR activity may compromise the ability of HSCs to sense environmental signals that allow these cells to balance quiescence, proliferation, migration, and differentiation. These data and others support a hypothesis that deregulation of AhR function has an important role in HSC regulation and in the etiology and/or progression of certain hematopoietic diseases, many of which are associated with aging.

Indexed as

Cell ProliferationGene Expression RegulationAnimalsCell CycleCell DifferentiationCell DivisionHematopoietic Stem CellsHumansImmunityMiceMice, KnockoutReceptors, Aryl HydrocarbonReceptors, Aryl HydrocarbonAh receptorhematopoietic stem cellsquiescence

Identifiers

PMID24495120
PMCPMC4923955
OpenAlexW1589175424

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.