Редактирование: OOEP (раздел)

==Publications==

{{medline-entry
|title=Maternal gene [i]Ooep[/i] may participate in homologous recombination-mediated DNA double-strand break repair in mouse oocytes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29955025
|abstract=DNA damage in oocytes can cause infertility and birth defects. DNA double-strand breaks (DSBs) are highly deleterious and can substantially impair genome integrity. Homologous recombination ([[HR]])-mediated DNA DSB repair plays dominant roles in safeguarding oocyte quantity and quality. However, little is known regarding the key players of the [[HR]] repair pathway in oocytes. Here, we identified oocyte-specific gene [i]Ooep[/i] as a novel key component of the [[HR]] repair pathway in mouse oocytes. [[OOEP]] was required for efficient ataxia telangiectasia mutated (ATM) kinase activation and Rad51 recombinase(RAD51)focal accumulation at DNA DSBs. [i]Ooep[/i] null oocytes were defective in DNA DSB repair and prone to apoptosis upon exogenous DNA damage insults. Moreover, [i]Ooep[/i] null oocytes exhibited delayed meiotic maturation. Therefore, [[OOEP]] played roles in preserving oocyte quantity and quality by maintaining genome stability. [i]Ooep[/i] expression decreased with the advance of maternal age, suggesting its involvement in maternal aging.
|mesh-terms=* Aging
* Animals
* DNA Breaks, Double-Stranded
* DNA Repair
* Female
* Meiosis
* Mice
* Mice, Inbred C57BL
* Oocytes
* RNA-Binding Proteins
* Recombination, Genetic
|keywords=* ATM
* DNA double-strand break repair
* Homologous recombination
* Ooep
* RAD51
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6085769
}}