ArticleProceedings of the National Academy of Sciences of the United States of America2001
High rate of CAD gene amplification in human cells deficient in MLH1 or MSH6.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
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- Targeting nucleotide metabolism as the nexus of viral infections, cancer, and the immune response.Science advances · 2021Review
- A Patient With CAD Deficiency Responsive to Uridine and Literature Review.Frontiers in neurology · 2020Article
- Small molecule activators of the p53 response.Journal of molecular cell biology · 2019Review
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- Repression of mutagenesis by Rad51D-mediated homologous recombination.Nucleic acids research · 2006Article
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- ATR functions as a gene dosage-dependent tumor suppressor on a mismatch repair-deficient background.The EMBO journal · 2004Article
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- Decreased expression of the DNA mismatch repair gene Mlh1 under hypoxic stress in mammalian cells.Molecular and cellular biology · 2003Article
- Embryonic stem cells and somatic cells differ in mutation frequency and type.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Caenorhabditis elegans DNA mismatch repair gene msh-2 is required for microsatellite stability and maintenance of genome integrity.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- DNA mismatch repair: molecular mechanism, cancer, and ageing.Mechanisms of ageing and developmentReview
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
MutS and MutL homologs have been implicated in multiple genetic stabilization pathways. The activities participate in the correction of DNA biosynthetic errors, are involved in cellular responses to certain types of DNA damage, and serve to ensure the fidelity of genetic recombination. We show here that the rate of CAD (carbamyl-P synthetase/aspartate transcarbamylase/dihydroorotase) gene amplification is elevated 50- to 100-fold in human cell lines deficient in MLH1 or MSH6, as compared with mismatch repair-proficient control cells. Fluorescence in situ hybridization indicates that these amplification events are the probable consequence of unequal sister chromatid exchanges involving chromosome 2, as well as translocation events involving other chromosomes. These results implicate MutS alpha and MutL alpha in the suppression of gene amplification and suggest that defects in this genetic stabilization function may contribute to the cancer predisposition associated with mismatch repair deficiency.
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