Evidence map›Paper›PMID 28520870›Full record

ArticleEndocrinology2017

Defining the Role of Estrogen Receptor β in the Regulation of Female Fertility.

M A Karim Rumi, Prabhakar Singh, Katherine F Roby, Xiao Zhao, Khursheed Iqbal, Anamika Ratri, Tianhua Lei, Wei Cui, Shaon Borosha, Pramod Dhakal and 5 more

Abstract read
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.6field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. [Mechanism ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Trial
  3. Article
  4. Review
  5. Article
  6. Methods for Defining the Role of ADAMTS1 in the Ovary.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  7. Frontiers in veterinary science · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

15 authors at 2 institutions in 1 country.

M A Karim RumiInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Prabhakar SinghInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Katherine F RobyInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Xiao ZhaoInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Khursheed IqbalInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Anamika RatriInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Tianhua LeiInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Wei CuiInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Shaon BoroshaInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Pramod DhakalInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Kaiyu KubotaInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Damayanti ChakrabortyInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Jay L VivianInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Michael W WolfeInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
Michael J SoaresInstitute for Reproductive Health and Regenerative Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160.
University of Kansas Medical Center · USInstitute for Reproductive Health · US

Funding

Transgenic and Gener-Targeting CoreP20GM104936 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SAADI, IRFAN · 2012 to 2016
$10.9M
Dissecting Uterine Progesterone ResistanceR21HD066406 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SOARES, MICHAEL J · 2012 to 2013
$404k
Rat Models for Sex Steroid ActionR21OD010478 · OD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SOARES, MICHAEL J · 2013 to 2014
$395k
NICHD NIH HHS R21 HD066406NIGMS NIH HHS P20 GM104936NIH HHS R21 OD010478
6 · The paper itself

Abstract

Estrogens are essential hormones for the regulation of fertility. Cellular responses to estrogens are mediated by estrogen receptor α (ESR1) and estrogen receptor β (ESR2). In mouse and rat models, disruption of Esr1 causes infertility in both males and females. However, the role of ESR2 in reproductive function remains undecided because of a wide variation in phenotypic observations among Esr2-mutant mouse strains. Regulatory pathways independent of ESR2 binding to its cognate DNA response element have also been implicated in ESR2 signaling. To clarify the regulatory roles of ESR2, we generated two mutant rat models: one with a null mutation (exon 3 deletion, Esr2ΔE3) and the other with an inframe deletion selectively disrupting the DNA binding domain (exon 4 deletion, Esr2ΔE4). In both models, we observed that ESR2-mutant males were fertile. ESR2-mutant females exhibited regular estrous cycles and could be inseminated by wild-type (WT) males but did not become pregnant or pseudopregnant. Esr2-mutant ovaries were small and differed from WT ovaries by their absence of corpora lutea, despite the presence of follicles at various stages of development. Esr2ΔE3- and Esr2ΔE4-mutant females exhibited attenuated preovulatory gonadotropin surges and did not ovulate in response to a gonadotropin regimen effective in WT rats. Similarities of reproductive deficits in Esr2ΔE3 and Esr2ΔE4 mutants suggest that DNA binding-dependent transcriptional function of ESR2 is critical for preovulatory follicle maturation and ovulation. Overall, the findings indicate that neuroendocrine and ovarian deficits are linked to infertility observed in Esr2-mutant rats.

Indexed as

AnimalsEstrogen Receptor betaFemaleFertilityGonadotropinsHEK293 CellsHeLa CellsHumansInfertility, FemaleMaleOvulationRatsRats, Sprague-DawleyRats, TransgenicEstrogen Receptor betaGonadotropins

Identifiers

PMID28520870
PMCPMC5505218
OpenAlexW2615648215

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.