ReviewBrain research2014
RNA-protein interactions in unstable microsatellite diseases.
Review in Brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 56 citations in OpenAlex.
- Distinct cellular effects of myotonic dystrophy type 2 repeat-associated non-AUG tetrapeptides.Disease models & mechanisms · 2026Article
- Nuclear MBL-1 modulates mitochondrial morphology through carnitine palmitoyltransferase inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Aberrant splicing exonizes C9orf72 repeat expansion in ALS/FTD.Nature neuroscience · 2025Article
- Application of antisense oligonucleotide drugs in amyotrophic lateral sclerosis and Huntington's disease.Translational neurodegeneration · 2025Review
- Alternative splicing dysregulation across tissue and therapeutic approaches in a mouse model of myotonic dystrophy type 1.Molecular therapy. Nucleic acids · 2024Article
- Modeling Myotonic Dystrophy Type 2 UsingInternational journal of molecular sciences · 2023Review
- Development of Therapeutic Approaches for Myotonic Dystrophies Type 1 and Type 2.International journal of molecular sciences · 2022Review
- Ribonuclease recruitment using a small molecule reduced c9ALS/FTD r(GScience translational medicine · 2021Article
- Article
- TCF4-mediated Fuchs endothelial corneal dystrophy: Insights into a common trinucleotide repeat-associated disease.Progress in retinal and eye research · 2021Review
- Targeted splice sequencing reveals RNA toxicity and therapeutic response in myotonic dystrophy.Nucleic acids research · 2021Article
- Brain Pathogenesis and Potential Therapeutic Strategies in Myotonic Dystrophy Type 1.Frontiers in aging neuroscience · 2021Review
- Insight Into Spinocerebellar Ataxia Type 31 (SCA31) FromFrontiers in neuroscience · 2021Review
- Nucleo-cytoplasmic transport defects and protein aggregates in neurodegeneration.Translational neurodegeneration · 2020Review
- A CRISPR-Cas13a Based Strategy That Tracks and Degrades Toxic RNA in Myotonic Dystrophy Type 1.Frontiers in genetics · 2020Article
- Structural insights into synthetic ligands targeting A-A pairs in disease-related CAG RNA repeats.Nucleic acids research · 2019Article
- Short Tandem Repeat Expansions and RNA-Mediated Pathogenesis in Myotonic Dystrophy.International journal of molecular sciences · 2019Review
- Repeat-Associated Non-ATG Translation: Molecular Mechanisms and Contribution to Neurological Disease.Annual review of neuroscience · 2019Review
- ADAR2 mislocalization and widespread RNA editing aberrations in C9orf72-mediated ALS/FTD.Acta neuropathologica · 2019Article
- Insights into C9ORF72-Related ALS/FTD from Drosophila and iPSC Models.Trends in neurosciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
A novel RNA-mediated disease mechanism has emerged from studies on dominantly inherited neurological disorders caused by unstable microsatellite expansions in non-coding regions of the genome. These non-coding tandem repeat expansions trigger the production of unusual RNAs that gain a toxic function, which involves the formation of RNA repeat structures that interact with, and alter the activities of, various factors required for normal RNA processing as well as additional cellular functions. In this review, we explore the deleterious effects of toxic RNA expression and discuss the various model systems currently available for studying RNA gain-of-function in neurologic diseases. Common themes, including bidirectional transcription and repeat-associated non-ATG (RAN) translation, have recently emerged from expansion disease studies. These and other discoveries have highlighted the need for further investigations designed to provide the additional mechanistic insights essential for future therapeutic development.
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.