ArticlePloS one2013
The role of 14-3-3ε interaction with phosphorylated Cdc25B at its Ser321 in the release of the mouse oocyte from prophase I arrest.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- The subcortical maternal complex modulates the cell cycle during early mammalian embryogenesis via 14-3-3.Nature communications · 2024Article
- Evidence of 14-3-3 proteins contributing to kinetochore integrity and chromosome congression during mitosis.Journal of cell science · 2024Article
- 14-3-3ε: a protein with complex physiology function but promising therapeutic potential in cancer.Cell communication and signaling : CCS · 2024Review
- Whole-Genome Re-sequencing and Transcriptome Reveal Oogenesis-Related Genes in Autotetraploid Carassius auratus.Marine biotechnology (New York, N.Y.) · 2021Article
- Hormesis of low-dose inhibition of pAkt1 (Ser473) followed by a great increase of proline-rich inositol polyphosphate 5-phosphatase (PIPP) level in oocytes.In vitro cellular & developmental biology. Animal · 2021Article
- Quantitative proteomic analysis of chicken serum reveals key proteins affecting follicle development during reproductive phase transitions.Poultry science · 2021Article
- Genotypic divergence in mouse oocyte transcriptomes: possible pathways to hybrid vigor impacting fertility and embryogenesis.Physiological genomics · 2020Article
- Intelligent Design of 14-3-3 Docking Proteins Utilizing Synthetic Evolution Artificial Intelligence (SYN-AI).ACS omega · 2019Article
- Involvement of CaMKII in regulating the release of diplotene-arrested mouse oocytes by pAkt1 (Ser473).Cell cycle (Georgetown, Tex.) · 2019Article
- YWHA (14-3-3) protein isoforms and their interactions with CDC25B phosphatase in mouse oogenesis and oocyte maturation.BMC developmental biology · 2019Article
- 14-3-3 Proteins: a window for a deeper understanding of fungal metabolism and development.World journal of microbiology & biotechnology · 2019Review
- Transcriptome profiling of human oocytes experiencing recurrent total fertilization failure.Scientific reports · 2018Article
- Differential abundance and transcription of 14-3-3 proteins during vegetative growth and sexual reproduction in budding yeast.Scientific reports · 2018Article
- Oxidative stress-induced DNA damage of mouse zygotes triggers G2/M checkpoint and phosphorylates Cdc25 and Cdc2.Cell stress & chaperones · 2016Article
- LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice.Nature communications · 2015Article
- 14-3-3 epsilon prevents G2/M transition of fertilized mouse eggs by binding with CDC25B.BMC developmental biology · 2014Article
- Proteomic analysis of cellular response induced by multi-walled carbon nanotubes exposure in A549 cells.PloS one · 2014Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protein kinase A (PKA)/Cdc25B pathway plays a critical role in maintaining meiotic arrest in mouse oocytes. However, the molecular mechanism underlying this interchange is not known. In this study, we assessed the role of 14-3-3ε interaction with phosphorylated Cdc25B at its Ser321 as the mouse oocyte is released from prophase I arrest. The 14-3-3ε isoform is a highly conserved protein with various regulatory roles, including maintenance of meiotic arrest. Cdc25B phosphatase is also a key cell cycle regulator. 14-3-3ε binds to Cdc25B-WT, which was abrogated when Ser321 of Cdc25B was mutated to Ala. In addition, we found that 14-3-3ε and Cdc25B were co-localized. Cdc25B was translocated from the cytoplasm to the nucleus shortly before germinal vesicle breakdown (GVBD) during the primary oocyte stage of oogenesis. However, mutation of Ser321 to Ala completely abolished the cytoplasmic localization of Cdc25B. Furthermore, oocytes co-expressing of Cdc25B-WT or Cdc25B-Ser321D and 14-3-3ε were unable to undergo GVBD. In contrast, co-expression of 14-3-3ε and Cdc25B-Ser321A induced GVBD and allowed the process to continue. Down-regulation of 14-3-3ε caused partial meiotic resumption. Taken together, these data indicate that Ser321 of Cdc25B is the specific binding site for 14-3-3ε binding, and that 14-3-3ε is the significant factor in Cdc25B regulation during meiotic resumption of GV stage.
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