ArticleMolecular and cellular biology2003
Long CTG tracts from the myotonic dystrophy gene induce deletions and rearrangements during recombination at the APRT locus in CHO cells.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Trinucleotide repeat instability during double-strand break repair: from mechanisms to gene therapy.Current genetics · 2019Review
- Cis- and Trans-Modifiers of Repeat Expansions: Blending Model Systems with Human Genetics.Trends in genetics : TIG · 2018Review
- RNA biology of disease-associated microsatellite repeat expansions.Acta neuropathologica communications · 2017Review
- DNA triplet repeat expansion and mismatch repair.Annual review of biochemistry · 2015Review
- Length-dependent CTG·CAG triplet-repeat expansion in myotonic dystrophy patient-derived induced pluripotent stem cells.Human molecular genetics · 2013Article
- Extrahelical (CAG)/(CTG) triplet repeat elements support proliferating cell nuclear antigen loading and MutLα endonuclease activation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- DNA base excision repair: a mechanism of trinucleotide repeat expansion.Trends in biochemical sciences · 2012Review
- Hsp90 modulates CAG repeat instability in human cells.Cell stress & chaperones · 2010Article
- Coordination between polymerase beta and FEN1 can modulate CAG repeat expansion.The Journal of biological chemistry · 2009Article
- Zinc-finger directed double-strand breaks within CAG repeat tracts promote repeat instability in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Mutation spectra in fragile X syndrome induced by deletions of CGG*CCG repeats.The Journal of biological chemistry · 2009Review
- Dnmt1 deficiency promotes CAG repeat expansion in the mouse germline.Human molecular genetics · 2008Article
- Genome-wide demethylation promotes triplet repeat instability independently of homologous recombination.DNA repair · 2008Article
- Long homopurine*homopyrimidine sequences are characteristic of genes expressed in brain and the pseudoautosomal region.Nucleic acids research · 2006Article
- 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
- Advances in mechanisms of genetic instability related to hereditary neurological diseases.Nucleic acids research · 2005Review
- Mechanistic features of CAG*CTG repeat contractions in cultured cells revealed by a novel genetic assay.Nucleic acids research · 2005Article
- Selectable system for monitoring the instability of CTG/CAG triplet repeats in mammalian cells.Molecular and cellular biology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Expansion of CTG triplet repeats in the 3' untranslated region of the DMPK gene causes the autosomal dominant disorder myotonic dystrophy. Instability of CTG repeats is thought to arise from their capacity to form hairpin DNA structures. How these structures interact with various aspects of DNA metabolism has been studied intensely for Escherichia coli and Saccharomyces cerevisiae but is relatively uncharacterized in mammalian cells. To examine the stability of (CTG)(17), (CTG)(98), and (CTG)(183) repeats during homologous recombination, we placed them in the second intron of one copy of a tandemly duplicated pair of APRT genes. Cells selected for homologous recombination between the two copies of the APRT gene displayed distinctive patterns of change. Among recombinants from cells with (CTG)(98) and (CTG)(183), 5% had lost large numbers of repeats and 10% had suffered rearrangements, a frequency more than 50-fold above normal levels. Analysis of individual rearrangements confirmed the involvement of the CTG repeats. Similar changes were not observed in proliferating (CTG)(98) and (CTG)(183) cells that were not recombinant at APRT. Instead, they displayed high frequencies of small changes in repeat number. The (CTG)(17) repeats were stable in all assays. These studies indicate that homologous recombination strongly destabilizes long tracts of CTG repeats.
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.