ArticleInternational journal of molecular medicine2018
SUMO2 modification of Aurora B and its impact on follicular development and atresia in the mouse ovary.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Mutation of the SUMOylation site of Aurora-B disrupts spindle formation and chromosome alignment in oocytes.Cell death discovery · 2024Article
- Chk1/2 inhibitor AZD7762 blocks the growth of preantral follicles by inducing apoptosis, suppressing proliferation, and interfering with the cell cycle in granulosa cells.Histology and histopathology · 2023Article
- Knockdown of Chk1 inhibits proliferation and promotes apoptosis in mouse granulosa cells and its regulation mechanism by miR-15a and miR-16.In vitro cellular & developmental biology. Animal · 2022Article
- Transcriptomic Data Analyses Reveal That Sow Fertility-Related lincRNAFrontiers in cell and developmental biology · 2021Article
- Aurora B prevents aneuploidy via MAD2 during the first mitotic cleavage in oxidatively damaged embryos.Cell proliferation · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the mammalian ovary, >99% follicles fail to ovulate due to apoptosis in granulosa cells. Aurora B, a core subunit enzyme of the chromosomal passenger complex, exerts a crucial role in microtubule‑kinetochore attachment, and has been reported to be modified by small ubiquitin‑related modifier (SUMO) proteins. However, the details of how Aurora B and its SUMOylation impact on follicular development have yet to be fully elucidated. The aim of the present study was to explore the roles, and possible molecular mechanism, of Aurora B and its SUMOylation in the granulosa cells of the mouse follicle. It was revealed that the protein level of Aurora B increased with follicular development and the growth of the granulosa cells. Aurora B impacted follicular development and atresia through mediating the p38 mitogen‑activated protein kinase and FasL/Fas pathways, and caused the downregulation of cyclin‑dependent kinase 4, proliferating cell nuclear antigen, Bcl‑2, and upregulation of caspases‑3 and ‑8 to modulate the viability of the granulosa cells. In addition, Aurora B undergoes modification by SUMO2, but not by SUMO1, in vivo and in vitro, and Lys‑207 is a major modification site. SUMOylation modulates follicular development through an increase in Aurora B localization in the nucleus, and by stabilizing the protein level of Aurora B and keeping the viability of the granulosa cells. Taken together, Aurora B and its SUMOylation are important for follicular development and atresia in the ovaries of mice.
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