Evidence map›Paper›PMID 22470123›Full record

ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2012

Ovarian abnormalities in a mouse model of fragile X primary ovarian insufficiency.

Gloria E Hoffman, Wei Wei Le, Ali Entezam, Noriyuki Otsuka, Zhi-Bin Tong, Lawrence Nelson, Jodi A Flaws, John H McDonald, Sanjeeda Jafar, Karen Usdin

Open access · bronzeAbstract read
In one paragraph

Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.2field-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, 73 citations in OpenAlex.

  1. Beyond Repetition: The Role of Gray Zone Alleles in the Upregulation ofInternational journal of molecular sciences · 2025
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  2. Review
  3. Population-based FMR1 carrier screening among reproductive women.Journal of assisted reproduction and genetics · 2024
    Article
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  13. Frontiers in molecular biosciences · 2020
    Review
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  15. 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

10 authors at 5 institutions in 2 countries.

Gloria E HoffmanDepartment of Biology, Morgan State University, Baltimore, MD 21251, USA. gl042@verizon.net
Wei Wei Le
Ali Entezam
Noriyuki Otsuka
Zhi-Bin Tong
Lawrence Nelson
Jodi A Flaws
John H McDonald
Sanjeeda Jafar
Karen Usdin
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USHokkaido University · JPMorgan State University · USNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Preconception Health and Reproductive Natural HistoryZIAHD000633 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI NELSON, LAWRENCE M · 2009 to 2016
$7.1M
Disease pathology in the Fragile X-associated disordersZIADK057809 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI USDIN, KAREN P. · 2009 to 2013
$1.6M
Intramural NIH HHS
6 · The paper itself

Abstract

FMR1 premutation (PM) alleles have 55-200 CGG·CCG-repeats in their 5' UTR. PM carriers are at risk of fragile X-associated tremor and ataxia syndrome (FXTAS). Females are also at risk for FX primary ovarian insufficiency (FXPOI). PM pathology is generally attributed to deleterious properties of transcripts with long CGG-tracts. For FXPOI, hormone changes suggest a reduced residual follicle pool. Whether this is due to a smaller than normal original follicle pool or an increased rate of follicle depletion is unclear. A FX-PM mouse the authors generated with 130 CGG·CCG-repeats in the endogenous Fmr1 gene recapitulates features of FXTAS. Here the authors demonstrate that the gross development of the ovary and the establishment of the primordial follicle pool is normal in these mice. However, these animals show a faster loss of follicles of all follicle classes, suggesting that the problem is intrinsic to the ovary. In addition, many oocytes show aberrant nuclear accumulation of FMRP and elevated levels of ubiquitination. Furthermore, PM follicles are smaller and have fewer granulosa cells (GCs) than normal. Thus, these animals have ovarian abnormalities involving both the oocytes and GCs that may shed light on the molecular basis of FXPOI in humans.

Indexed as

AnimalsCell CountDisease Models, AnimalFemaleFollicular AtresiaFragile X Messenger Ribonucleoprotein 1Granulosa CellsMiceMice, Inbred C57BLMice, Mutant StrainsOocytesOrgan SpecificityOvarian FollicleOvaryPrimary Ovarian InsufficiencyUbiquitinationFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1

Identifiers

PMID22470123
PMCPMC3393073
OpenAlexW2043301688

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.