ReviewAmerican journal of human genetics1999
Myotonic dystrophy: the role of RNA CUG triplet repeats.
Review in American journal of human genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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.
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Who cites it
24 citing papers in PubMed.
- Elevated Levels of Active GSK3β in the Blood of Patients with Myotonic Dystrophy Type 1 Correlate with Muscle Weakness.International journal of molecular sciences · 2025Article
- Structural and Dynamical Properties of Nucleic Acid Hairpins Implicated in Trinucleotide Repeat Expansion Diseases.Biomolecules · 2024Review
- Personalized mRNA vaccines in glioblastoma therapy: from rational design to clinical trials.Journal of nanobiotechnology · 2024Review
- Development of Therapeutic Approaches for Myotonic Dystrophies Type 1 and Type 2.International journal of molecular sciences · 2022Review
- Correction of RNA-Binding Protein CUGBP1 and GSK3β Signaling as Therapeutic Approach for Congenital and Adult Myotonic Dystrophy Type 1.International journal of molecular sciences · 2019Review
- Correction of GSK3β at young age prevents muscle pathology in mice with myotonic dystrophy type 1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Reduction of toxic RNAs in myotonic dystrophies type 1 and type 2 by the RNA helicase p68/DDX5.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Molecular mechanisms of muscle atrophy in myotonic dystrophies.The international journal of biochemistry & cell biology · 2013Review
- Daytime sleepiness and myotonic dystrophy.Current neurology and neuroscience reports · 2013Review
- GSK3β is a new therapeutic target for myotonic dystrophy type 1.Rare diseases (Austin, Tex.) · 2013Article
- GSK3β mediates muscle pathology in myotonic dystrophy.The Journal of clinical investigation · 2012Article
- Molecular, physiological, and motor performance defects in DMSXL mice carrying >1,000 CTG repeats from the human DM1 locus.PLoS genetics · 2012Article
- RNA Foci, CUGBP1, and ZNF9 are the primary targets of the mutant CUG and CCUG repeats expanded in myotonic dystrophies type 1 and type 2.The American journal of pathology · 2011Article
- Daytime sleepiness and REM sleep characteristics in myotonic dystrophy: a case-control study.Sleep · 2011Article
- Expansion of CUG RNA repeats causes stress and inhibition of translation in myotonic dystrophy 1 (DM1) cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Myotonic dystrophies 1 and 2: complex diseases with complex mechanisms.Current genomics · 2010Article
- Repeat expansion disease: progress and puzzles in disease pathogenesis.Nature reviews. Genetics · 2010Review
- Structural basis for the sequence-specific RNA-recognition mechanism of human CUG-BP1 RRM3.Nucleic acids research · 2009Article
- Reduction of the rate of protein translation in patients with myotonic dystrophy 2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- RNA structure of trinucleotide repeats associated with human neurological diseases.Nucleic acids research · 2003Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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.