ArticleCell death & disease2024
TMEM232 is required for the formation of sperm flagellum and male fertility in mice.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- DUET-seq: An Open-Source Droplet Platform for High-Fidelity Joint Chromatin and Transcriptome Profiling Reveals Temporal Regulatory Decoupling in Single Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single Intraperitoneal Busulfan Injection Induces Long-Term Reproductive Dysfunction and Reduces Male Offspring Ratio in BALB/c Mice.Journal of applied toxicology : JAT · 2026Article
- DNA methylation clock in bull sperm cells reveals the epigenetic aging characteristics and impact on fertility.Journal of animal science and biotechnology · 2026Article
- Mutations in CFAP57 disrupt the localization of MYH10 and IFT88, leading to flagellogenesis failure in humans and mice.Human genomics · 2025Article
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Authors and funding
17 authors.
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Abstract
Asthenoteratozoospermia is a major cause of male infertility. Thus far, the identified related genes can explain only a small share of asthenoteratozoospermia cases, suggesting the involvement of other genes. The transmembrane protein TMEM232 is highly expressed in mouse testes. In the present study, to determine its function of TMEM232 in testes, we constructed a Tmem232-null mouse model using CRISPR-Cas9 technology. Tmem232 knockout (KO) male mice was completely infertile, and their sperm were immotile, with morphological defects of the flagellum. Electron microscopy revealed an aberrant midpiece-principal junction and the loss of the fourth outer microtubule doublet in the sperm of Tmem232
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