ArticleNature medicine2009
Inhibition of the c-Abl-TAp63 pathway protects mouse oocytes from chemotherapy-induced death.
Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 2 of them syntheses that pooled it.
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Who cites it
189 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025Pooled it
- Molecular regulation of DNA damage and repair in female infertility: a systematic review.Reproductive biology and endocrinology : RB&E · 2024Pooled it
- In vivo labeling-based proteomic analysis of early follicle oocytes and cisplatin-induced alterations in mice.Nature communications · 2026Article
- Mesenchymal stem cell therapy for premature ovarian insufficiency: progress and challenges.Journal of ovarian research · 2026Review
- DNA damage response signaling in oocytes from an oncofertility perspective†.Biology of reproduction · 2026Review
- Fertility under fire: how chemotherapy harms the ovaries and the science fighting back?Journal of ovarian research · 2026Review
- Fertility Protection in Female Cancer Patients: From Molecular Mechanisms of Gonadotoxic Therapies to Pharmacotherapeutic Possibilities.International journal of molecular sciences · 2025Review
- Deletion of p63 exon 13 in mice reveals C-terminal isoform-specific functions in epithelial development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Effect of Imatinib Mesylate on the Ovarian Reserves of Female Patients with Chronic Myeloid Leukaemia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025Article
- Does gonadotoxic chemotherapy deplete the ovarian reserve through activation of primordial follicles?Human reproduction (Oxford, England) · 2025Article
- Chromatin remodeler CHD4 establishes chromatin states required for ovarian reserve formation, maintenance and male germ cell survival.Nucleic acids research · 2025Article
- Extensive homologous recombination safeguards oocyte genome integrity in mammals.Nucleic acids research · 2025Article
- p63: A Master Regulator at the Crossroads Between Development, Senescence, Aging, and Cancer.Cells · 2025Review
- Management of CML and Pregnancy in Low-and Middle-income Countries.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025Review
- Targeting programmed cell death with natural products: a potential therapeutic strategy for diminished ovarian reserve and fertility preservation.Frontiers in pharmacology · 2025Review
- An overview of different methods to establish a murine premature ovarian failure model.Animal models and experimental medicine · 2024Review
- Oocyte death is triggered by the stabilization of TAp63α dimers in response to cisplatin.Cell death & disease · 2024Article
- Fertility protection during chemotherapy treatment by boosting the NAD(P)EMBO molecular medicine · 2024Article
- Histological assessment for investigation of dose-dependent ovarian toxicity of cyclophosphamide in the rat.Heliyon · 2024Article
- Review
129 more citing papers are in PubMed but not listed here.
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Funding
Abstract
Germ cells are sensitive to genotoxins, and ovarian failure and infertility are major side effects of chemotherapy in young patients with cancer. Here we describe the c-Abl-TAp63 pathway activated by chemotherapeutic DNA-damaging drugs in model human cell lines and in mouse oocytes and its role in cell death. In cell lines, upon cisplatin treatment, c-Abl phosphorylates TAp63 on specific tyrosine residues. Such modifications affect p63 stability and induce a p63-dependent activation of proapoptotic promoters. Similarly, in oocytes, cisplatin rapidly promotes TAp63 accumulation and eventually cell death. Treatment with the c-Abl kinase inhibitor imatinib counteracts these cisplatin-induced effects. Taken together, these data support a model in which signals initiated by DNA double-strand breaks are detected by c-Abl, which, through its kinase activity, modulates the p63 transcriptional output. Moreover, they suggest a new use for imatinib, aimed at preserving oocytes of the follicle reserve during chemotherapeutic treatments.
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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.