Paper Publications
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[1] Genetic deficiency of EXOSC10 ribonuclease disrupts spermatogenesis and male fertility in mice. J Biol Chem, 2025.
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[2] . Exosc10 deficiency in the initial segment is dispensable for sperm maturation and male fertility in mice. ZYGOTE, 2024.
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[3] Conditional ablation of DIS3L2 ribonuclease in pre-meiotic germ cells causes defective spermatogenesis and infertility in male mice. Theranostics, 2024.
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[4] Loss of DIS3L in the initial segment is dispensable for sperm maturation in the epididymis and male fertility. Reproductive Biology, 2024.
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[5] DIS3 ribonuclease is essential for spermatogenesis and male fertility in mice. Development, 2024.
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[6] MAGE-B4, a binding partner of PRAMEF12, is dispensable for spermatogenesis and male fertility in mice. Biochemical and Biophysical Research Communications, 675, 46-53, 2023.
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[7] Epididymal DIS3 exosome ribonuclease is not necessary for mouse sperm maturation or fertility. Biochemical and Biophysical Research Communications, 666, 36-44, 2023.
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[8] Transcriptome profiling of the initial segment and proximal caput of mouse epididymis. Frontiers in Endocrinology, 14, 2023.
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[9] FIGLA, LHX8 and SOHLH1 transcription factor networks regulate mouse oocyte growth and differentiation. Nucleic Acids Research, 2020.
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[10] scRNA-seq Profiling of Human Testes Reveals the Presence of the ACE2 Receptor, A Target for SARS-CoV-2 Infection in Spermatogonia, Leydig and Sertoli Cells. Cells, 2020.
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[11] Sertoli cell-only phenotype and scRNA-seq define PRAMEF12 as a factor essential for spermatogenesis in mice. Nature Communications, 2019.
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[12] Transforming growth factor-β signaling participates in the maintenance of the primordial follicle pool in the mouse ovary. Journal of Biological Chemistry, 2014.
