ArticleOncogene2004
p53 functions in the incorporation step in DNA base excision repair in mouse liver mitochondria.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 98 citations in OpenAlex.
- Expression of p53 and p63 proteins and their correlation with histological grades among gastric carcinoma specimens at Mbarara Regional Referral Hospital.African journal of laboratory medicine · 2026Article
- Review
- Nuclear-Mitochondrial Interactions.Biomolecules · 2022Review
- Down-regulation of TFAM increases the sensitivity of tumour cells to radiation via p53/TIGAR signalling pathway.Journal of cellular and molecular medicine · 2019Article
- The effects of AICAR and rapamycin on mitochondrial function in immortalized mitochondrial DNA mutator murine embryonic fibroblasts.Biology open · 2018Article
- Emerging Roles of p53 Family Members in Glucose Metabolism.International journal of molecular sciences · 2018Review
- Knockout of Mpv17-Like Protein (M-LPH) Gene in Human Hepatoma Cells Results in Impairment of mtDNA Integrity through Reduction of TFAM, OGG1, and LIG3 at the Protein Levels.Oxidative medicine and cellular longevity · 2018Article
- The Δ133p53 Isoform Reduces Wtp53-induced Stimulation of DNA Pol γ Activity in the Presence and Absence of D4T.Aging and disease · 2017Article
- p53 in the mitochondria, as a trans-acting protein, provides error-correction activities during the incorporation of non-canonical dUTP into DNA.Oncotarget · 2016Article
- LACE1 interacts with p53 and mediates its mitochondrial translocation and apoptosis.Oncotarget · 2016Article
- TP53 mutation, mitochondria and cancer.Current opinion in genetics & development · 2016Review
- Amelioration of premature aging in mtDNA mutator mouse by exercise: the interplay of oxidative stress, PGC-1α, p53, and DNA damage. A hypothesis.Current opinion in genetics & development · 2016Review
- p53 as guardian of the mitochondrial genome.FEBS letters · 2016Review
- Bridged Analogues for p53-Dependent Cancer Therapy Obtained by S-Alkylation.International journal of peptide research and therapeutics · 2016Article
- Differential Protein Distribution between the Nucleus and Mitochondria: Implications in Aging.Frontiers in genetics · 2016Review
- Mitochondrial DNA maintenance: an appraisal.Molecular and cellular biochemistry · 2015Review
- p53 and mitochondrial function in neurons.Biochimica et biophysica acta · 2014Review
- Tumor suppressor p53 and estrogen receptors in nuclear-mitochondrial communication.Mitochondrion · 2014Review
- Protein folding as a driving force for dual protein targeting in eukaryotes.Frontiers in molecular biosciences · 2014Review
- Base-excision repair activity of uracil-DNA glycosylase monitored using the latch zone of α-hemolysin.Journal of the American Chemical Society · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor suppressor p53 protein stimulates nuclear base excision repair (BER) in vitro. In response to certain cellular stresses, p53 translocates to mitochondria, where it can trigger an apoptotic response. However, a potential role for p53 in modulating mitochondrial DNA repair has not yet been examined. In this study, we show that p53 also modulates mitochondrial BER. Uracil-initiated BER incorporation, which measures flux through the entire BER pathway, was lower in mitochondrial extracts from nonstressed p53 knockout mice than in wild type. The addition of recombinant p53 complemented the BER incorporation in p53 knockout extracts and stimulated BER in wt extracts. The activities of three major mitochondrial DNA glycosylases were similar in extracts from wild-type and knockout animals. Likewise, AP endonuclease activity was unaffected by the absence of p53. Gel shift experiments with recombinant p53 demonstrated that p53 did not bind to the uracil-containing substrate used in the repair assay. Polymerase gamma gap-filing activity was less efficient in p53 knockout extracts, but it was complemented with the addition of recombinant p53. Thus, we conclude that p53 may participate in mtBER by stimulating the repair synthesis incorporation step.
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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.