ArticleMolecular and cellular biology2003
Selectable system for monitoring the instability of CTG/CAG triplet repeats in mammalian 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 24 papers.
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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.
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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.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- A distal promoter and aberrant splicing enable canonical translation of out-of-frame proteins in Huntington's disease.bioRxiv : the preprint server for biology · 2025Article
- Cas9 nickase-mediated contractions of CAG/CTG repeats are transcription-dependent and replication-independent.NAR molecular medicine · 2024Article
- DNA Base Damage Repair Crosstalks with Chromatin Structures to Contract Expanded GAA Repeats in Friedreich's Ataxia.Biomolecules · 2024Article
- CAG repeat expansions create splicing acceptor sites and produce aberrant repeat-containing RNAs.Molecular cell · 2024Article
- CAG repeat expansions create splicing acceptor sites and produce aberrant repeat-containing RNAs.bioRxiv : the preprint server for biology · 2023Article
- Expanded CAG/CTG repeats resist gene silencing mediated by targeted epigenome editing.Human molecular genetics · 2022Article
- Modifiers of CAG/CTG Repeat Instability: Insights from Mammalian Models.Journal of Huntington's disease · 2021Review
- Suppression of Mutant Protein Expression in SCA3 and SCA1 Mice Using a CAG Repeat-Targeting Antisense Oligonucleotide.Molecular therapy. Nucleic acids · 2019Article
- Break-induced replication sparks CGG-repeat instability.Nature structural & molecular biology · 2018Article
- Mechanisms of genetic instability caused by (CGG)Nature structural & molecular biology · 2018Article
- Highly specific contractions of a single CAG/CTG trinucleotide repeat by TALEN in yeast.PloS one · 2014Article
- Article
- Topoisomerase 1 and single-strand break repair modulate transcription-induced CAG repeat contraction in human cells.Molecular and cellular biology · 2011Article
- Convergent transcription through a long CAG tract destabilizes repeats and induces apoptosis.Molecular and cellular biology · 2010Article
- Hsp90 modulates CAG repeat instability in human cells.Cell stress & chaperones · 2010Article
- Trinucleotide repeats in human genome and exome.Nucleic acids research · 2010Article
- Diverse effects of individual mismatch repair components on transcription-induced CAG repeat instability in human cells.DNA repair · 2009Article
- Instability and chromatin structure of expanded trinucleotide repeats.Trends in genetics : TIG · 2009Review
- 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
- Transcription destabilizes triplet repeats.Molecular carcinogenesis · 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Despite substantial progress in understanding the mechanism by which expanded CTG/CAG trinucleotide repeats cause neurodegenerative diseases, little is known about the basis for repeat instability itself. By taking advantage of a novel phenomenon, we have developed a selectable assay to detect contractions of CTG/CAG triplets. When inserted into an intron in the APRT gene or the HPRT minigene, long tracts of CTG/CAG repeats (more than about 33 repeat units) are efficiently incorporated into mRNA as a new exon, thereby rendering the encoded protein nonfunctional, whereas short repeat tracts do not affect the phenotype. Therefore, contractions of long repeats can be monitored in large cell populations, by selecting for HPRT(+) or APRT(+) clones. Using this selectable system, we determined the frequency of spontaneous contractions and showed that treatments with DNA-damaging agents stimulate repeat contractions. The selectable system that we have developed provides a versatile tool for the analysis of CTG/CAG repeat instability in mammalian cells. We also discuss how the effect of long CTG/CAG repeat tracts on splicing may contribute to the progression of polyglutamine diseases.
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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.