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Obox1 deficiency induceds subfertility in female mice

GSE207448 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/07/02 Platform GPL17021
Summary
Obox1 was considered to be a maternal factor participates in oogenesis and follicle development, but its function remains largely undefined. In this study, we demonstrated that Obox1-null female mice displayed subfertility as evidenced by decreased litter size. Obox1 deficiency resulted in less oocytes production. The levels of female sex hormones and gonadotropins, especially luteinizing hormone (LH), were significantly decreased both in ovaries and serum at diestrus. Further studies showed that Obox1-null ovaries were hypo-reactive to LH. There are still more unruptured follicles in the ovaries after superovulation in Obox1-null ovaries. The number of corpus luteum (CL) and serum concentration of progesterone (P4) reduced, and the steroidogenesis-related genes were aberrant in Obox1-null mice. In conclusion, Obox1 deficiency impaired ovulation and luteinization and led to female subfertility.
Published in
Obox1 deficiency impairs fertility in female mice
Wu L, Shen J, Hou Z et al. · Fundamental research 2025 · PMID 40777786 · doi:10.1016/j.fmre.2025.04.008
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Also filed as BioProject PRJNA855632 and SRA study SRP384878. Searching any of these in the dataset finder brings you back here.

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