ArticleNucleic acids research1992
A mechanism for deletion formation in DNA by human cell extracts: the involvement of short sequence repeats.
Article in Nucleic acids research, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Association of mitochondrial DNA variations with lung cancer risk in a Han Chinese population from southwestern China.PloS one · 2012Article
- Efficiency of nonhomologous DNA end joining varies among somatic tissues, despite similarity in mechanism.Cellular and molecular life sciences : CMLS · 2011Article
- Base damage immediately upstream from double-strand break ends is a more severe impediment to nonhomologous end joining than blocked 3'-termini.Radiation research · 2011Article
- Anti-apoptotic protein BCL2 down-regulates DNA end joining in cancer cells.The Journal of biological chemistry · 2010Article
- Nonhomologous DNA end joining in cell-free extracts.Journal of nucleic acids · 2010Article
- Non-homologous DNA end joining in normal and cancer cells and its dependence on break structures.Genetics and molecular biology · 2010Article
- Microhomology-mediated end joining in fission yeast is repressed by pku70 and relies on genes involved in homologous recombination.Genetics · 2007Article
- Double-strand breaks in the myotonic dystrophy type 1 and the fragile X syndrome triplet repeat sequences induce different types of mutations in DNA flanking sequences in Escherichia coli.Nucleic acids research · 2006Article
- Analysis of 5' junctions of human LINE-1 and Alu retrotransposons suggests an alternative model for 5'-end attachment requiring microhomology-mediated end-joining.Genome research · 2005Article
- Review
- Gene rearrangements induced by the DNA double-strand cleaving agent neocarzinostatin: conservative non-homologous reciprocal exchanges in an otherwise stable genome.Nucleic acids research · 2002Article
- Development of a novel rapid assay to assess the fidelity of DNA double-strand-break repair in human tumour cells.Nucleic acids research · 2002Article
- Twin priming: a proposed mechanism for the creation of inversions in L1 retrotransposition.Genome research · 2001Article
- The role of DNA polymerase activity in human non-homologous end joining.Nucleic acids research · 2001Article
- DNA-binding and strand-annealing activities of human Mre11: implications for its roles in DNA double-strand break repair pathways.Nucleic acids research · 2001Article
- DNA double-strand break repair in cell-free extracts from Ku80-deficient cells: implications for Ku serving as an alignment factor in non-homologous DNA end joining.Nucleic acids research · 2000Article
- Microdeletions in FMR2 may be a significant cause of premature ovarian failure.Journal of medical genetics · 1999Article
- Modification of non-conservative double-strand break (DSB) rejoining activity after the induction of cisplatin resistance in human tumour cells.British journal of cancer · 1999Article
- Radiation-induced chromosome aberrations in Saccharomyces cerevisiae: influence of DNA repair pathways.Genetics · 1998Article
- Non-homologous DNA end joining in plant cells is associated with deletions and filler DNA insertions.Nucleic acids research · 1997Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA molecules carrying a site-specific double-strand break were exposed to nuclear extracts from human cell lines. It was shown previously that breaks could be rejoined correctly by human extracts, but that a proportion of the rejoined molecules had suffered deletions and insertions. The 'mis-rejoined' proportion was higher with cell extracts from an individual with the disorder ataxia-telangiectasia than with normal cell extracts. We now show by sequence analysis that deletions in extract-treated molecules occur exclusively between short direct repeats (2-6 base pairs). A mis-rejoined molecule containing an insertion of 300 bp also had a repeat-based deletion at the same site. A number of different direct repeats are involved; however, some clustering of these occurs especially on the upstream side of the initial breakpoint. These data are most simply interpreted in terms of a model of deletion formation involving single-strand exposure and repair, perhaps with the action of other DNA-metabolising enzymes influencing the frequency with which some repeats are involved.
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