ArticleProceedings of the National Academy of Sciences of the United States of America1995
p53 deficiency does not affect the accumulation of point mutations in a transgene target.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 81 citations in OpenAlex.
- The rate of spontaneous mutations in human myeloid cells.Mutation research · 2013Article
- Unbalanced replication as a major source of genetic instability in cancer cells.American journal of blood research · 2012Article
- BAX and tumor suppressor TRP53 are important in regulating mutagenesis in spermatogenic cells in mice.Biology of reproduction · 2010Article
- Tumour suppression by p53: a role for the DNA damage response?Nature reviews. Cancer · 2009Review
- DNA repair dysfunction in gastrointestinal tract cancers.Cancer science · 2008Review
- Article
- Modeling variation in tumors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Elevated mutagenesis and decreased DNA repair at a transgene are associated with proliferation but not apoptosis in p53-deficient cells.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Review
- Physical and functional interactions of the tumor suppressor protein p53 and DNA polymerase alpha-primase.Nucleic acids research · 2002Article
- Selective inactivation of p53 facilitates mouse epithelial tumor progression without chromosomal instability.Molecular and cellular biology · 2001Article
- Chromosome instability contributes to loss of heterozygosity in mice lacking p53.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Dissociation of p53-mediated suppression of homologous recombination from G1/S cell cycle checkpoint control.Oncogene · 2000Article
- Article
- P53-dependent and -independent links between DNA-damage, apoptosis and mutation frequency in ES cells.Oncogene · 1999Article
- Tumors of DNA mismatch repair-deficient hosts exhibit dramatic increases in genomic instability.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Stochastic modelling of tumorigenesis in p53 deficient mice.British journal of cancer · 1998Article
- p53 is phosphorylated by CDK7-cyclin H in a p36MAT1-dependent manner.Molecular and cellular biology · 1997Article
- p53-mediated protective responses to UV irradiation.Proceedings of the National Academy of Sciences of the United States of America · 1997Review
- Illegitimate recombination leading to allelic loss and unbalanced translocation in p53-mutated human lymphoblastoid cells.Molecular and cellular biology · 1997Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
DNA repair is required by organisms to prevent the accumulation of mutations and to maintain the integrity of genetic information. Mammalian cells that have been treated with agents that damage DNA have an increase in p53 levels, a p53-dependent arrest at G1 in the cell cycle, and a p53-dependent apoptotic response. It has been hypothesized that this block in cell cycle progression is necessary to allow time for DNA repair or to direct the damaged cell to an apoptotic pathway. This hypothesis predicts that p53-deficient cells would have an abnormal apoptotic response and exhibit a "mutator" phenotype. Using a sensitive assay for the accumulation of point mutations, small deletions, and insertions, we have directly tested whether p53-deficient cells exhibit an increased frequency of mutation before and after exposure to DNA-damaging agents. We report that wild-type and p53-deficient fibroblasts, thymocytes, and tumor tissue have indistinguishable rates of point mutation accumulation in a transgenic lacI target gene. These results suggest that the role of p53 in G1 checkpoint control and tumor suppression does not affect the accumulation of point mutations.
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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.