Evidence map›Paper›PMID 21384534›Full record

ArticleBirth defects research. Part A, Clinical and molecular teratology2011

Epigenetic control of embryonic renal cell differentiation by L1 retrotransposon.

Kenneth S Ramos, Diego E Montoya-Durango, Ivo Teneng, Adrian Nanez, Vilius Stribinskis

Open access · greenAbstract read
In one paragraph

Article in Birth defects research. Part A, Clinical and molecular teratology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 23 citations in OpenAlex.

  1. New insights on anti-tumor immunity of CD8Journal of translational medicine · 2025
    Review
  2. Review
  3. Article
  4. Article
  5. New Trends in Aryl Hydrocarbon Receptor Biology.Frontiers in cell and developmental biology · 2016
    Review
  6. Article
  7. Article
  8. AHR regulates WT1 genetic programming during murine nephrogenesis.Molecular medicine (Cambridge, Mass.) · 2011
    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.

Kenneth S RamosDepartment of Biochemistry and Molecular Biology and Center for Genetics and Molecular Medicine, School of Medicine, University of Louisville, Louisville, KY 40202, USA. Kenneth.ramos@louisville.edu
Diego E Montoya-Durango
Ivo Teneng
Adrian Nanez
Vilius Stribinskis
University of Louisville · USUniversity of Louisville Hospital · US

Funding

Strategic Vision & Impact on Environmental HealthP30ES014443 · NIEHS · UNIVERSITY OF LOUISVILLE · PI PROUGH, RUSSELL ALLEN · 2007 to 2010
$4.4M
MOLECULAR MECHANISMS OF VASCULAR TOXICITYR01ES004849 · NIEHS · UNIVERSITY OF LOUISVILLE · PI RAMOS, KENNETH S · 1988 to 2005
$1.3M
NIEHS NIH HHS 5R01 ES004849NIEHS NIH HHS ES014443NIEHS NIH HHS P30 ES014443NIEHS NIH HHS R01 ES004849
6 · The paper itself

Abstract

backgroundL1 retroelements may play a central role in morphogenesis through epigenetic mechanisms involving recruitment of chromatin modifying protein complexes. Retroelements are repressed in terminally differentiated cells, and highly active in embryonic, undifferentiated, and transformed cells. It is not clear if the modulation of differentiation by L1 is a "cause" or "effect". The purpose of this study was to determine if murine embryonic kidney cells of clonal origin (mK4 cells) harbor retrotransposition events upon ectopic expression of L1, and the impact of L1 on embryonic kidney cell differentiation. Given that L1 is reactivated by aryl hydrocarbon receptor (AHR) ligands, we also sought to investigate the effects of benzo(a)pyrene (BaP) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the genetic network of mK4 cells.

methodsThe mK4 cells overexpressing human L1(RP) were assessed for changes in proliferation and expression of molecular markers of cellular differentiation.

resultsL1(RP) increased proliferation rates and markedly downregulated differentiation programming in mK4 cells. These genetic alterations were recapitulated by exogenous activation of L1 by AHR ligands.

conclusionL1 regulates nephrogenesis in vitro via both insertional and non-insertional mechanisms that disrupt mesenchymal to epithelial transition. Thus, a feedback loop involving L1, WT1, and AHR may play a role in regulation of kidney morphogenesis. Birth Defects Research (Part A), 2011. © 2011 Wiley-Liss, Inc.

Indexed as

Cell DifferentiationEpigenesis, GeneticGene Expression Regulation, DevelopmentalAnimalsBenzo(a)pyreneCell ProliferationCells, CulturedGene Regulatory NetworksKidneyMiceMorphogenesisPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRetroelementsBenzo(a)pyrenePolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRetroelements

Identifiers

PMID21384534
PMCPMC3180906
OpenAlexW2113371388

What OpenQuestion holds

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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.