ReviewFEBS letters2016
p53 as guardian of the mitochondrial genome.
Review in FEBS letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 140 citations in OpenAlex.
- The Senescent Phenotype of Cultured Hypothalamic Astrocytes from Rats with Streptozotocin-Induced Dementia.Neurochemical research · 2026Article
- The Interaction of Structural Analogues of Phenothiazines in p53-Dependent Cellular Signaling Pathways.ACS omega · 2026Article
- The significance of mitochondrial DNA changes during the onset and progression of head and neck squamous cell carcinoma.Future oncology (London, England) · 2026Review
- p53 and PD-1/PD-L1 expression contribute to disease progression and are correlated to immune infiltrates in urothelial carcinoma.Scientific reports · 2025Article
- Endocrine disruption to metastasis: How phthalates promote breast carcinogenesis.Ecotoxicology and environmental safety · 2025Review
- New 1,2,4-Triazole Derivatives with aInternational journal of molecular sciences · 2025Article
- Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025Review
- Article
- Ubiquitin: Not just a one-way ticket to the proteasome, but a therapeutic dial to fine-tune the molecular landscape of disease.Clinical and translational medicine · 2024Review
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- From Cell Populations to Molecular Complexes: Multiplexed Multimodal Microscopy to Explore p53-53BP1 Molecular Interaction.International journal of molecular sciences · 2024Article
- A mechanistic biomarker investigation of fialuridine hepatotoxicity using the chimeric TK-NOG Hu-liver mouse model and in vitro micropatterned hepatocyte cocultures.Toxicology research · 2024Article
- Cardiovascular aging: spotlight on mitochondria.American journal of physiology. Heart and circulatory physiology · 2024Review
- Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions.Frontiers in endocrinology · 2024Review
- Increased cancer risk in HIV-infected individuals occupationally exposed to chemicals: Depression of p53 as the key driver.PLOS global public health · 2024Article
- USP39 attenuates the antitumor activity of cisplatin on colon cancer cells dependent on p53.Cell biology and toxicology · 2023Article
- Downregulation of PI3K/AKT/mTOR Pathway in Juglone-Treated Bovine Oocytes.Antioxidants (Basel, Switzerland) · 2023Article
- Advances in exercise to alleviate sarcopenia in older adults by improving mitochondrial dysfunction.Frontiers in physiology · 2023Review
- Elevation of effective p53 expression sensitizes wild-type p53 breast cancer cells to CDK7 inhibitor THZ1.Cell communication and signaling : CCS · 2022Article
- Tumor suppressor p53 restrains cancer cell dissemination by modulating mitochondrial dynamics.Oncogenesis · 2022Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Participating in the repair of nuclear DNA is one mechanism by which p53 suppresses tumorigenesis, but there is growing evidence that p53 also helps maintain the mitochondrial genome through its translocation into mitochondria and interactions with mtDNA repair proteins. Because of the susceptibility of mtDNA to oxidative damage and replication errors, it is vital to protect mtDNA genomic stability to preserve health and fitness. Here, we focus on reviewing the evidence for the involvement of p53 in maintaining the integrity of mtDNA through its activities in both the nucleus and the mitochondria.
Indexed as
Identifiers
What OpenQuestion holds
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.