ArticleReproductive biology and endocrinology : RB&E2024
Fance deficiency impaired DNA damage repair of prospermatogonia and altered the repair dynamics of spermatocytes.
Article in Reproductive biology and endocrinology : RB&E, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The Role of Whole Exome Sequencing in the Genetic Evaluation of the Infertile Man.Advances in experimental medicine and biology · 2026Review
- The vaginal microbiome of transgender men receiving gender-affirming hormonal therapy in comparison to that of cisgender women.Scientific reports · 2024Article
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Authors and funding
3 authors.
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Abstract
backgroundNon-obstructive azoospermia (NOA) is the most severe form of male infertility and affects approximately 1% of men worldwide. Fanconi anemia (FA) genes were known for their essential role in DNA repair and growing evidence showed the crucial role of FA pathway in NOA. However, the underlying mechanisms for Fance deficiency lead to a serious deficit and delayed maturation of male germ cells remain unclear.
methodsWe used Fance deficiency mouse model for experiments, and collected testes or epididymides from mice at 8 weeks (8W), 17.5 days post coitum (dpc), and postnatal 11 (P11) to P23. The mice referred to three genotypes: wildtype (Fance
resultsIn the present study, we found that the adult male Fance
conclusionsFance deficiency caused massive male germ cell loss involved in the imbalance of DNA damage repair in prospermatogonia and altered dynamics of proteins in homologous recombination, DNA end resection, and crossover, providing new insights into the etiology and molecular basis of NOA.
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