Evidence map›Paper›PMID 24983622›Full record

ArticlePloS one2014

Identification of sites of STAT3 action in the female reproductive tract through conditional gene deletion.

Rebecca L Robker, Laura N Watson, Sarah A Robertson, Kylie R Dunning, Eileen A McLaughlin, Darryl L Russell

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. pSTAT3 activation ofProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. STAT3 Is an Upstream Regulator ofInternational journal of molecular sciences · 2021
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Genes · 2018
    Article
  12. Gene networks for total number born in pigs across divergent environments.Mammalian genome : official journal of the International Mammalian Genome Society · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

6 authors at 2 institutions in 1 country.

Rebecca L RobkerRobinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, South Australia, Australia.
Laura N WatsonRobinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, South Australia, Australia.
Sarah A RobertsonRobinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, South Australia, Australia.
Kylie R DunningRobinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, South Australia, Australia.
Eileen A McLaughlinSchool of Environmental & Life Sciences, University of Newcastle, Callaghan, New South Wales, Australia.
Darryl L RussellRobinson Research Institute, School of Paediatrics and Reproductive Health, The University of Adelaide, Adelaide, South Australia, Australia.
University of Adelaide · AUUniversity of Newcastle Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The STAT3 transcription factor is a pleiotropic transducer of signalling by hormones, growth factors and cytokines that has been identified in the female reproductive tract from oocytes and granulosa cells of the ovary to uterine epithelial and stromal cells. In the present study we used transgenic models to investigate the importance of STAT3 for reproductive performance in these different tissues. The Cre-LoxP system was used to delete STAT3 in oocytes by crossing Stat3fl/fl with Zp3-cre+ mice, or in ovarian granulosa cells and uterine stroma by crossing with Amhr2-Cre+ mice. Surprisingly, deletion of STAT3 in oocytes had no effect on fertility indicating that the abundance of STAT3 protein in maturing oocytes and fertilized zygotes is not essential to these developmental stages. In Stat3fl/fl;Amhr2-cre+ females impaired fertility was observed through significantly fewer litters and smaller litter size. Ovulation rate, oocyte fertilization and development to blastocyst were unaffected in this line; however, poor recombination efficiency in granulosa cells had yielded no net change in STAT3 protein abundance. In contrast, uteri from these mice showed STAT3 protein depletion selectively from the stomal compartment. A significant reduction in number of viable fetuses on gestational day 18, increased fetal resorptions and disrupted placental morphology were evident causes of the reduced fertility. In conclusion, this study defines an important role for STAT3 in uterine stromal cells during embryo implantation and the development of a functional placenta.

Indexed as

Gene DeletionAnimalsFemaleGenitalia, FemaleInfertility, FemaleMaleMiceSTAT3 Transcription FactorStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID24983622
PMCPMC4077744
OpenAlexW1971913712

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.