ReviewGenes2020
Antisense Transcription across Nucleotide Repeat Expansions in Neurodegenerative and Neuromuscular Diseases: Progress and Mysteries.
Review in Genes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 17 citations in OpenAlex.
- Regulation of PHOX2B gene expression by the long non-coding natural antisense RNA PHOX2B-AS1.The FEBS journal · 2026Article
- Repeat-associated non-AUG translation as a common mechanism for the polyGln ataxias.Cell reports · 2026Article
- RNA dysregulation in neurodegenerative diseases.The EMBO journal · 2025Review
- The RNA Revolution in the Central Molecular Biology Dogma Evolution.International journal of molecular sciences · 2024Review
- Decoding Nucleotide Repeat Expansion Diseases: Novel Insights fromInternational journal of molecular sciences · 2024Review
- Statistical Genomics Analysis of Simple Sequence Repeats from the Paphiopedilum Malipoense Transcriptome Reveals Control Knob Motifs Modulating Gene Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- RNA as a component of scrapie fibrils.Scientific reports · 2024Article
- Structure and Alternative Splicing of the Antisense FMR1 (ASFMR1) Gene.Molecular neurobiology · 2023Article
- Aberrant phase separation is a common killing strategy of positively charged peptides in biology and human disease.bioRxiv : the preprint server for biology · 2023Article
- Review
- Molecular Therapies for Myotonic Dystrophy Type 1: From Small Drugs to Gene Editing.International journal of molecular sciences · 2022Review
- Review
- Non-coding RNAs in chromatin folding and nuclear organization.Cellular and molecular life sciences : CMLS · 2021Review
- Special Issue "Genetic Advances in Neuromuscular Disorders: From Gene Identification to Gene Therapy".Genes · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unstable repeat expansions and insertions cause more than 30 neurodegenerative and neuromuscular diseases. Remarkably, bidirectional transcription of repeat expansions has been identified in at least 14 of these diseases. More remarkably, a growing number of studies has been showing that both sense and antisense repeat RNAs are able to dysregulate important cellular pathways, contributing together to the observed clinical phenotype. Notably, antisense repeat RNAs from spinocerebellar ataxia type 7, myotonic dystrophy type 1, Huntington's disease and frontotemporal dementia/amyotrophic lateral sclerosis associated genes have been implicated in transcriptional regulation of sense gene expression, acting either at a transcriptional or posttranscriptional level. The recent evidence that antisense repeat RNAs could modulate gene expression broadens our understanding of the pathogenic pathways and adds more complexity to the development of therapeutic strategies for these disorders. In this review, we cover the amazing progress made in the understanding of the pathogenic mechanisms associated with repeat expansion neurodegenerative and neuromuscular diseases with a focus on the impact of antisense repeat transcription in the development of efficient therapies.
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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.