ArticleCell death & disease2018
Ablation of beta subunit of protein kinase CK2 in mouse oocytes causes follicle atresia and premature ovarian failure.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Ceramide: a pivotal lipid mediator shaping female reproductive homeostasis and pathophysiology.Journal of ovarian research · 2026Review
- Analysis of the resistance of small peptides from Periplaneta americana to HScientific reports · 2026Article
- Protein phosphatase 4 maintains the survival of primordial follicles by regulating autophagy in oocytes.Cell death & disease · 2024Article
- Mechanism of Zuogui pill enhancing ovarian function and skin elastic repair in premature aging rats based on artificial intelligence medical image analysis.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Therapeutic effects of human umbilical cord mesenchymal stem cell-derived extracellular vesicles on ovarian functions through the PI3K/Akt cascade in mice with premature ovarian failure.European journal of histochemistry : EJH · 2023Article
- The Activation of Reticulophagy by ER Stress through the ATF4-MAP1LC3A-CCPG1 Pathway in Ovarian Granulosa Cells Is Linked to Apoptosis and Necroptosis.International journal of molecular sciences · 2023Article
- Comparative miRNA expression profile analysis of porcine ovarian follicles: new insights into the initiation mechanism of follicular atresia.Frontiers in genetics · 2023Article
- Current understanding of the genomic abnormities in premature ovarian failure: chance for early diagnosis and management.Frontiers in medicine · 2023Review
- TGF-β1 regulates the lncRNA transcriptome of ovarian granulosa cells in a transcription activity-dependent manner.Cell proliferation · 2023Article
- p63 expression in granulosa-luteinized cells of infertile patients with peritoneal endometriosis submitted to in vitro fertilization.JBRA assisted reproduction · 2022Article
- EpCAM deficiency causes premature aging of intestinal epithelium via hyperactivating mTORC1 pathway.Clinical and translational medicine · 2022Article
- Beneficial Effects of Traditional Chinese Medicine in the Treatment of Premature Ovarian Failure.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- METTL3-mediated mRNA NCell death & disease · 2021Article
- NORHA, a novel follicular atresia-related lncRNA, promotes porcine granulosa cell apoptosis via the miR-183-96-182 cluster and FoxO1 axis.Journal of animal science and biotechnology · 2021Article
- The Role of Mutant p63 in Female Fertility.International journal of molecular sciences · 2021Review
- Therapeutic Role of Mesenchymal Stem Cell-Derived Extracellular Vesicles in Female Reproductive Diseases.Frontiers in endocrinology · 2021Review
- Deletion of Ck2β gene causes germ cell development arrest and azoospermia in male mice.Cell proliferation · 2020Article
- Casein kinase 2 modulates the spindle assembly checkpoint to orchestrate porcine oocyte meiotic progression.Journal of animal science and biotechnology · 2020Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Premature ovarian failure (POF), a major cause of female infertility, is a complex disorder, but the molecular mechanisms underlying the disorder are only poorly understood. Here we report that protein kinase CK2 contributes to maintaining follicular survival through PI3K/AKT pathway and DNA damage response pathway. Targeted deletion of CK2β in mouse oocytes from the primordial follicle stage resulted in female infertility, which was attributed to POF incurring by massive follicle atresia. Downregulated PI3K/AKT signaling was found after CK2β deletion, indicated by reduced level of phosphorylated AKT (S473, T308, and S129) and altered AKT targets related to cell survival. Further studies discovered that CK2β-deficient oocytes showed enhanced γH2AX signals, indicative of accumulative unrepaired DSBs, which activated CHK2-dependant p53 and p63 signaling. The suppressed PI3K/AKT signaling and failed DNA damage response signaling probably contribute to large-scale oocyte loss and eventually POF. Our findings provide important new clues for elucidating the mechanisms underlying follicle atresia and POF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.