ReviewJournal of Huntington's disease2018
A Fresh Look at Huntingtin mRNA Processing in Huntington's Disease.
Review in Journal of Huntington's disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 22 citations in OpenAlex.
- ELLA: modeling subcellular spatial variation of gene expression within cells in high-resolution spatial transcriptomics.Nature communications · 2025Article
- Update on the Symptomatic Treatment of Huntington's Disease: From Pathophysiology to Clinical Practice.International journal of molecular sciences · 2025Review
- Bento: a toolkit for subcellular analysis of spatial transcriptomics data.Genome biology · 2024Article
- Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021Review
- Neurodegenerative diseases: a hotbed for splicing defects and the potential therapies.Translational neurodegeneration · 2021Review
- MicroRNAs in Huntington's Disease: Diagnostic Biomarkers or Therapeutic Agents?Frontiers in cellular neuroscience · 2021Review
- Nemo-like kinase reduces mutant huntingtin levels and mitigates Huntington's disease.Human molecular genetics · 2020Article
- Huntingtin Lowering Strategies.International journal of molecular sciences · 2020Review
- Comparison of the Huntington's Disease like 2 and Huntington's Disease Clinical Phenotypes.Movement disorders clinical practice · 2019Article
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 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) is an inherited neurodegenerative disorder caused by a mutation that expands the polyglutamine (CAG) repeat in exon 1 of the huntingtin (HTT) gene. Wild-type HTT protein interacts with other proteins to protect cells against toxic stimuli, mediate vesicle transport and endocytosis, and modulate synaptic activity. Mutant HTT protein disrupts autophagy, vesicle transport, neurotransmitter signaling, and mitochondrial function. Although many of the activities of wild-type HTT protein and the toxicities of mutant HTT protein are characterized, less is known about the activities of HTT mRNA. Most putative HD therapies aim to target mutant HTT mRNA before it is translated into the protein. Therefore, it is imperative to learn as much as we can about how cells handle both wild-type and mutant HTT mRNA so that effective therapies can be designed. Here, we review the structure of wild-type and mutant HTT mRNA, with emphasis on their alternatively polyadenylated or spliced isoforms. We then consider the abundance of HTT mRNA isoforms in HD and discuss the potential implications of these findings. Evidence in the review should be used to guide future research aimed at developing mRNA-lowering therapies for HD.
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.