ArticlePloS one2016
Primary Ovarian Insufficiency Induced by Fanconi Anemia E Mutation in a Mouse Model.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- Integrated analysis of FANCE expression and its regulatory role in the immune microenvironment of oral squamous cell carcinoma.Oncology letters · 2025Article
- Identifying therapeutic targets for primary ovarian insufficiency through integrated genomic analyses.Journal of ovarian research · 2024Article
- Fance deficiency impaired DNA damage repair of prospermatogonia and altered the repair dynamics of spermatocytes.Reproductive biology and endocrinology : RB&E · 2024Article
- Fance deficiency inhibits primordial germ cell proliferation associated with transcription-replication conflicts accumulate and DNA repair defects.Journal of ovarian research · 2023Article
- Selected Genetic Factors Associated with Primary Ovarian Insufficiency.International journal of molecular sciences · 2023Review
- Pan-cancer analysis of the prognostic and immunological role of Fanconi anemia complementation group E.Frontiers in genetics · 2022Article
- Genomic Consideration in Chemotherapy-Induced Ovarian Damage and Fertility Preservation.Genes · 2021Review
- Review
- Essential Role of BRCA2 in Ovarian Development and Function.The New England journal of medicine · 2018Article
- Dearth and Delayed Maturation of Testicular Germ Cells in Fanconi Anemia E Mutant Male Mice.PloS one · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In most cases of primary ovarian insufficiency (POI), the cause of the depletion of ovarian follicles is unknown. Fanconi anemia (FA) proteins are known to play important roles in follicular development. Using random insertional mutagenesis with a lentiviral transgene, we identified a family with reduced fertility in the homozygous transgenic mice. We identified the integration site and found that the lentivirus had integrated into intron 8 of the Fanconi E gene (Fance). By RT-PCR and in situ hybridization, we found that Fance transcript levels were significantly reduced. The Fance homozygous mutant mice were assayed for changes in ovarian development, follicle numbers and estrous cycle. Ovarian dysplasias and a severe lack of follicles were seen in the mutant mice. In addition, the estrous cycle was disrupted in adult females. Our results suggest that POI has been induced by the Fance mutation in this new mouse model.
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Registered trials
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.