ArticleGenetics2020
Oocyte Elimination Through DNA Damage Signaling from CHK1/CHK2 to p53 and p63.
Article in Genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Loss of Nemp1 disrupts female meiosis and activates a conserved ATM-CHK2 checkpoint.Nature communications · 2026Article
- Slowing down the clock on ovarian aging-does the ovary hold the secret to the fountain of youth?GeroScience · 2026Review
- Later age of natural menopause among women with the pathogenicJournal of medical genetics · 2026Article
- DNMT/TET Imbalance and Network-Level DNA Methylation Remodeling in Ovarian Aging: Mechanistic Perspectives.Biology · 2026Review
- TRIP13 fosters both transcriptional silencing and DSB repair during meiosis.bioRxiv : the preprint server for biology · 2025Article
- CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve.The Journal of cell biology · 2025Article
- Research progress on the adverse effects of high-altitude environment to the male reproductive system: a review study.Frontiers in endocrinology · 2025Review
- Premeiotic deletion of Eif2s2 causes oocyte arrest at the early diplotene stage and apoptosis in mice.Cell proliferation · 2024Article
- Defects in meiosis I contribute to the genesis of androgenetic hydatidiform moles.The Journal of clinical investigation · 2024Article
- Primary oocytes with cellular senescence features are involved in ovarian aging in mice.Scientific reports · 2024Article
- Amentoflavone reverses epithelial-mesenchymal transition in hepatocellular carcinoma cells by targeting p53 signalling pathway axis.Journal of cellular and molecular medicine · 2024Article
- BRCA1 safeguards genome integrity by activating chromosome asynapsis checkpoint to eliminate recombination-defective oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- TP63 truncating mutation causes increased cell apoptosis and premature ovarian insufficiency by enhanced transcriptional activation of CLCA2.Journal of ovarian research · 2024Article
- Primary oocytes with cellular senescence features are involved in ovarian aging in mice.bioRxiv : the preprint server for biology · 2024Article
- Heat shock factor 5 establishes the male germ-line meiotic sex chromosome inactivation through regulation ofHeliyon · 2023Article
- Checkpoint Kinase 1 Is a Key Signal Transducer of DNA Damage in the Early Mammalian Cleavage Embryo.International journal of molecular sciences · 2023Review
- DNA Double-Strand Break-Related Competitive Endogenous RNA Network of Noncoding RNA in Bovine Cumulus Cells.Genes · 2023Article
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
- Inhibition of EED activity enhances cell survival of female germline stem cell and improves the oocytes production during oogenesisOpen biology · 2023Article
- The dual role of p63 in cancer.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Eukaryotic organisms have evolved mechanisms to prevent the accumulation of cells bearing genetic aberrations. This is especially crucial for the germline, because fecundity and fitness of progeny would be adversely affected by an excessively high mutational incidence. The process of meiosis poses unique problems for mutation avoidance because of the requirement for SPO11-induced programmed double-strand breaks (DSBs) in recombination-driven pairing and segregation of homologous chromosomes. Mouse meiocytes bearing unrepaired meiotic DSBs or unsynapsed chromosomes are eliminated before completing meiotic prophase I. In previous work, we showed that checkpoint kinase 2 (CHK2; CHEK2), a canonical DNA damage response protein, is crucial for eliminating not only oocytes defective in meiotic DSB repair (
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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.