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Ubiquitin C‐terminal hydrolase L1 (UCHL1), a double‐edged sword in mammalian oocyte maturation and spermatogenesis

Background Recent studies have shown that ubiquitin‐mediated cell apoptosis can modulate protein interaction and involve in the progress of oocyte maturation and spermatogenesis. As one of the key regulators involved in ubiquitin signal, ubiquitin C‐terminal hydrolase L1 (UCHL1) is considered a mole...

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Published in:Cell proliferation 2023-02, Vol.56 (2), p.e13347-n/a
Main Authors: Yang, Donghui, Lu, Qizhong, Peng, Sha, Hua, Jinlian
Format: Article
Language:English
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Summary:Background Recent studies have shown that ubiquitin‐mediated cell apoptosis can modulate protein interaction and involve in the progress of oocyte maturation and spermatogenesis. As one of the key regulators involved in ubiquitin signal, ubiquitin C‐terminal hydrolase L1 (UCHL1) is considered a molecular marker associated with spermatogonia stem cells. However, the function of UCHL1 was wildly reported to regulate various bioecological processes, such as Parkinson's disease, lung cancer, breast cancer and colon cancer, how UCHL1 affects the mammalian reproductive system remains an open question. Methods We identified papers through electronic searches of PubMed database from inception to July 2022. Results Here, we summarize the important function of UCHL1 in controlling mammalian oocyte development, regulating spermatogenesis and inhibiting polyspermy, and we posit the balance of UCHL1 was essential to maintaining reproductive cellular and tissue homeostasis. Conclusion This study considers the ‘double‐edged sword’ role of UCHL1 during gametogenesis and presents new insights into UCHL1 in germ cells. UCHL1 and mammalian gametogenesis. UCHL1 affects apoptosis‐related factors in mammalian gametogenesis and controls mammalian oocyte development, regulates spermatogenesis and inhibits polyspermy. It may also have other biological functions in the testis or ovary, such as anti‐inflammatory or antiviral.
ISSN:0960-7722
1365-2184
1365-2184
DOI:10.1111/cpr.13347