ArticleGenetics2000
Mutation frequency and specificity with age in liver, bladder and brain of lacI transgenic mice.
Article in Genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 104 citations in OpenAlex.
- Biomarkers of aging.Science China. Life sciences · 2023Review
- From DNA damage to mutations: All roads lead to aging.Ageing research reviews · 2021Review
- Cellular parabiosis and the latency of age-related diseases.Open biology · 2019Review
- New Possibilities on the Horizon: Genome Editing Makes the Whole Genome Accessible for Changes.Frontiers in plant science · 2019Review
- Somatic Mutagenesis in Mammals and Its Implications for Human Disease and Aging.Annual review of genetics · 2018Review
- DNA mismatch repair preferentially protects genes from mutation.Genome research · 2018Article
- Recombinant cells in the lung increase with age via de novo recombination events and clonal expansion.Environmental and molecular mutagenesis · 2017Article
- Early age decline in DNA repair capacity in the liver: in depth profile of differential gene expression.Aging · 2016Article
- Article
- DNA double strand break repair, aging and the chromatin connection.Mutation research · 2016Review
- Epigenetic reduction of DNA repair in progression to gastrointestinal cancer.World journal of gastrointestinal oncology · 2015Article
- Novel diet-related mouse model of colon cancer parallels human colon cancer.World journal of gastrointestinal oncology · 2014Article
- How ageing processes influence cancer.Nature reviews. Cancer · 2013Review
- Sirtuin 6 (SIRT6) rescues the decline of homologous recombination repair during replicative senescence.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- A mouse model of accelerated liver aging caused by a defect in DNA repair.Hepatology (Baltimore, Md.) · 2012Article
- Cellular stress response pathways and ageing: intricate molecular relationships.The EMBO journal · 2011Review
- Metabolism, genomics, and DNA repair in the mouse aging liver.Current gerontology and geriatrics research · 2011Article
- Polk mutant mice have a spontaneous mutator phenotype.DNA repair · 2009Article
- Altered senescence, apoptosis, and DNA damage response in a mutant p53 model of accelerated aging.Mechanisms of ageing and development · 2009Article
- Bladder cancer in the elderly: clinical outcomes, basic mechanisms, and future research direction.Nature clinical practice. Urology · 2009Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutation frequency and specificity were determined as a function of age in nuclear DNA from liver, bladder, and brain of Big Blue lacI transgenic mice aged 1.5-25 months. Mutations accumulated with age in liver and accumulated more rapidly in bladder. In the brain a small initial increase in mutation frequency was observed in young animals; however, no further increase was observed in adult mice. To investigate the origin of mutations, the mutational spectra for each tissue and age were determined. DNA sequence analysis of mutant lacI transgenes revealed no significant changes in mutational specificity in any tissue at any age. The spectra of mutations found in aging animals were identical to those in younger animals, suggesting that they originated from a common set of DNA lesions manifested during DNA replication. The data also indicated that there were no significant age-related mutational changes due to oxidative damage, or errors resulting from either changes in the fidelity of DNA polymerase or the efficiency of DNA repair. Hence, no evidence was found to support hypotheses that predict that oxidative damage or accumulation of errors in nuclear DNA contributes significantly to the aging process, at least in these three somatic tissues.
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.