Evidence map›Paper›PMID 20032047›Full record

ArticleEndocrinology2010

The follistatin-288 isoform alone is sufficient for survival but not for normal fertility in mice.

Fuminori Kimura, Yisrael Sidis, Lara Bonomi, Yin Xia, Alan Schneyer

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Follistatin Alleviates Hepatic Steatosis in NAFLD via the mTOR Dependent Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Article
  3. Review
  4. Article
  5. A non-coding region nearProceedings. Biological sciences · 2018
    Article
  6. Follistatin is critical for mouse uterine receptivity and decidualization.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  7. Activins and Inhibins: Roles in Development, Physiology, and Disease.Cold Spring Harbor perspectives in biology · 2016
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. The Local Control of the Pituitary by Activin Signaling and Modulation.Open neuroendocrinology journal (Online) · 2011
    Article
  18. Article
  19. 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.

Fuminori KimuraPioneer Valley Life Science Institute, 3601 Main Street, Springfield, Massachusetts 01107, USA.
Yisrael Sidis
Lara Bonomi
Yin Xia
Alan Schneyer
University of Massachusetts Amherst · USMassachusetts General Hospital · US

Funding

Physiologic Roles of Activin and Myostatin AntagonistsR01DK075058 · NIDDK · UNIVERSITY OF MASSACHUSETTS AMHERST · PI SCHNEYER, ALAN L · 2007 to 2010
$774k
Regulation Of Follicle Development and Fertility By Activin and FollistatinR21HD062859 · NICHD · UNIVERSITY OF MASSACHUSETTS AMHERST · PI SCHNEYER, ALAN L · 2010 to 2011
$450k
NICHD NIH HHS 21HD062859NICHD NIH HHS R21 HD062859NIDDK NIH HHS R01 DK075058NIDDK NIH HHS R01DK075058
6 · The paper itself

Abstract

Follistatin (FST) is a natural antagonist of activin and related TGFbeta superfamily ligands that exists as three protein isoforms differing in length at the C terminus. The longest FST315 isoform is found in the circulation, whereas the shortest FST288 isoform is typically found in or on cells and tissues, and the intermediate FST303 isoform is found in gonads. We recently demonstrated that the FST isoforms have distinct biological actions in vitro that, taken together with the differential distribution, suggests they may also have different roles in vivo. To explore the specific role of individual FST isoforms, we created a single-isoform FST288-only mouse. In contrast to the neonatal death of FST global knockout mice, FST288-only mice survive to adulthood. Although they appear normal, FST288-only mice have fertility defects including reduced litter size and frequency. Follicles were counted in ovaries from 8.5- to 400-d-old females. Significantly fewer morphologically healthy antral follicles were found in 100- to 250-d FST288-only ovaries, but there were significantly more secondary, primary, and primordial follicles detected at d 8.5 in FST288-only ovaries. However, depletion of this primordial follicle pool is more rapid in FST288-only females resulting in a deficit by 250 d of age and early cessation of reproduction. Superovulated FST288-only females have fewer ovulated eggs and embryos. These results indicate that the FST isoforms have different activities in vivo, that the FST288-only isoform is sufficient for development, and that loss of FST303 and FST315 isoforms results in fertility defects that resemble activin hyperactivity and premature ovarian failure.

Indexed as

Embryonic DevelopmentFertilityReproductionAnimalsFemaleFollistatinMiceOvaryProtein IsoformsFollistatinfollistatin, 288-amino acid isoformProtein Isoforms

Identifiers

PMID20032047
PMCPMC2840692
OpenAlexW2071410270

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.