Evidence map›Paper›PMID 24607249›Full record

ReviewReproductive biology2014

Estrogen hormone physiology: reproductive findings from estrogen receptor mutant mice.

Katherine J Hamilton, Yukitomo Arao, Kenneth S Korach

Open access · greenAbstract readReview
In one paragraph

Review in Reproductive biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 157 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Current Insights in Prolactin Signaling and Ovulatory Function.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Article
  16. Review
  17. The evolutionary impact and influence of oestrogens on adipose tissue structure and function.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  18. Article
  19. Article
  20. Article

11 more citing papers are in PubMed but not listed here.

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.

Katherine J HamiltonReceptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences/NIH, Research Triangle Park, NC 27709, United States.
Yukitomo AraoReceptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences/NIH, Research Triangle Park, NC 27709, United States.
Kenneth S KorachReceptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences/NIH, Research Triangle Park, NC 27709, United States. Electronic address: Korach@niehs.nih.gov.
National Institute of Environmental Health Sciences · US

Funding

Chemical Receptor Interactions In Reproduction And Hormonal ToxicityZIAES070065 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KORACH, KENNETH S · 2009 to 2019
$29.6M
NIEHS Knock Out Mouse Core (KOMC) Annual ReportZICES102425 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RAY, MANAS · 2010 to 2025
$20.1M
Intramural NIH HHS ZIA ES070065
6 · The paper itself

Abstract

Estrogen receptors (ERs) play a crucial role in reproduction and normal physiology. The two sub-types of ER (ERα and β) are expressed in various levels in different tissues and selective cell types. Gene targeting technology allowed us to produce lines of mice with disrupted ERα (αERKO) and ERβ genes (βERKO) as well as a compound αβERKO in the whole body. Male and female αERKO mice are infertile. Estrogen, EGF and IGF-1 treatments failed to induce uterine growth and DNA synthesis in αERKO uteri. αERKO females are infertile due to hypoplastic uteri and hyperemic ovaries with no corpora lutea due to persistent LH stimulation from loss of negative feedback. αERKO males are infertile, with testicular atrophy and seminiferous tubule dysmorphogenesis producing decreased spermatogenesis and inactive sperm. βERKO females show arrested folliculogenesis and subfertility. Ovarian analyses indicate differential gene expression related to ovulatory stimulation deficits including lack of LH, PR, Cyp19 and Cox2 expression. A unique ovarian phenotype is found only in αβERKO females showing transdifferentiation of granulosa cells to Sertoli cells. We describe here several novel mouse models which possess ERα gene modification. To understand ERα function in uterine endometrial epithelial cells, we generated a tissue selective ERα gene disrupted mouse model, the uterine epithelial-specific ERα knockout (UtEpiαERKO). To understand the physiological role of ERα functional domains, we generated a mouse model with a mutation in the ligand dependent transcription activation domain of ERα (AF2ERKI). Findings from the ERα mutant mice suggest that the absence of functional ERα is not lethal and results in significant endocrine effects and altered physiological processes.

Indexed as

Mice, KnockoutAnimalsEstrogen Receptor alphaEstrogen Receptor betaEstrogensFemaleFertilityMaleMiceOvaryEstrogen Receptor alphaEstrogen Receptor betaEstrogensEstrogen receptorFertilityGenetically modified mouseOvaryTransactivation functionUterus

Identifiers

PMID24607249
PMCPMC4777324
OpenAlexW2006115622

What OpenQuestion holds

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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.