ArticleeLife2016
Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 70 citations in OpenAlex.
- Loss of Nemp1 disrupts female meiosis and activates a conserved ATM-CHK2 checkpoint.Nature communications · 2026Article
- Isoform-specific cofactor recruitment through the intrinsically disordered N-terminus of p63 underlies differential transcriptional activities.bioRxiv : the preprint server for biology · 2026Article
- Evaluating Selective Quality Control in Mammalian Oogenesis: Evidence and Opportunities.Annual review of genetics · 2025Review
- Alternative splicing in the DBD linker region of p63 modulates binding to DNA and iASPP in vitro.Cell death & disease · 2025Article
- Differential Transcriptional Activity of ΔNp63β Is Encoded by an Isoform-Specific C-Terminus.Molecular and cellular biology · 2025Article
- Crosstalk between paralogs and isoforms influences p63-dependent regulatory element activity.Nucleic acids research · 2024Article
- Advances in the genetic etiology of female infertility.Journal of assisted reproduction and genetics · 2024Review
- Oocyte death is triggered by the stabilization of TAp63α dimers in response to cisplatin.Cell death & disease · 2024Article
- Context dependent activity of p63-bound gene regulatory elements.bioRxiv : the preprint server for biology · 2024Article
- Molecular Mechanisms Determining Mammalian Oocyte Quality with the Treatment of Cancer Therapy.Advances in anatomy, embryology, and cell biology · 2024Review
- Fuzzy interactions between the auto-phosphorylated C-terminus and the kinase domain of CK1δ inhibits activation of TAp63α.Scientific reports · 2023Article
- Heterozygous TP63 pathogenic variants in isolated primary ovarian insufficiency.Journal of assisted reproduction and genetics · 2023Article
- Disease-related p63 DBD mutations impair DNA binding by distinct mechanisms and varying degree.Cell death & disease · 2023Article
- Mitochondria in reproduction.Clinical and experimental reproductive medicine · 2023Article
- Designed Ankyrin Repeat Proteins as a tool box for analyzing p63.Cell death and differentiation · 2022Article
- The Splicing Factor PTBP1 RepressesCancer research communications · 2022Article
- Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis.Cell reports · 2022Article
- ASH1L contributes to oocyte apoptosis by regulating DNA damage.American journal of physiology. Cell physiology · 2022Article
- Dominant TP63 missense variants lead to constitutive activation and premature ovarian insufficiency.Human mutation · 2022Article
- Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022Review
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction.
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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.