Evidence map›Paper›PMID 19812388›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2009

Selective disruption of ER{alpha} DNA-binding activity alters uterine responsiveness to estradiol.

Sylvia C Hewitt, Jeanne E O'Brien, J Larry Jameson, Grace E Kissling, Kenneth S Korach

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Estrogen Hormone Biology.Current topics in developmental biology · 2017
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. The role of genetics in estrogen responses: a critical piece of an intricate puzzle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Review
  16. Article
  17. Article
  18. 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

5 authors at 4 institutions in 1 country.

Sylvia C HewittNational Institute of Environment Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA. curtiss@niehs.nih.gov
Jeanne E O'Brien
J Larry Jameson
Grace E Kissling
Kenneth S Korach
Northwestern University · USNational Institute of Environmental Health Sciences · USNational Institutes of Health · USResearch Triangle Park Foundation · US

Funding

Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Chemical Receptor Interactions In Reproduction And Hormonal ToxicityZIAES070065 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KORACH, KENNETH S · 2009 to 2019
$29.6M
Transition Metal Regulation of Oocyte MaturationP01HD021921 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MAYO, KELLY E · 1987 to 2013
$18.5M
NIEHS Statistical Consulting ServiceZIAES045005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PEDDADA, SHYAMAL · 2009 to 2011
$2.8M
Intramural NIH HHSNICHD NIH HHS P01 HD021921NICHD NIH HHS P01 HD21921
6 · The paper itself

Abstract

In vitro models have been used to demonstrate that estrogen receptors (ERs) can regulate estrogen-responsive genes either by directly interacting with estrogen-responsive element (ERE) DNA motifs or by interacting with other transcription factors such as AP1. In this study, we evaluated estrogen (E(2))-dependent uterine gene profiles by microarray in the KIKO mouse, an in vivo knock-in mouse model that lacks the DNA-binding function of ERalpha and is consequently restricted to non-ERE-mediated responses. The 2- or 24-h E(2)-mediated uterine gene responses were distinct in wild-type (WT), KIKO, and alphaERKO genotypes, indicating that unique sets of genes are regulated by ERE and non-ERE pathways. After 2 h E(2) treatment, 38% of the WT transcripts were also regulated in the KIKO, demonstrating that the tethered mechanism does operate in this in vivo model. Surprisingly, 1438 E(2)-regulated transcripts were unique in the KIKO mouse and were not seen in either WT or alphaERKO. Pathway analyses revealed that some canonical pathways, such as the Jak/Stat pathway, were affected in a similar manner by E(2) in WT and KIKO. In other cases, however, the WT and KIKO differed. One example is the Wnt/beta-catenin pathway; this pathway was impacted, but different members of the pathway were regulated by E(2) or were regulated in a different manner, consistent with differences in biological responses. In summary, this study provides a comprehensive analysis of uterine genes regulated by E(2) via ERE and non-ERE pathways.

Indexed as

Animalsbeta CateninDNAEstradiolEstrogen Receptor alphaEstrogensFemaleMiceMice, Mutant StrainsOligonucleotide Array Sequence AnalysisOvariectomyPoint MutationProtein BindingReverse Transcriptase Polymerase Chain ReactionSignal TransductionUterusbeta CateninDNAEstradiolEstrogen Receptor alphaEstrogensWnt Proteins

Identifiers

PMID19812388
PMCPMC2796155
OpenAlexW2038447064

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.