ReviewCurrent opinion in genetics & development2014
The expanding role for chromatin and transcription in polyglutamine disease.
Review in Current opinion in genetics & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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
19 citing papers in PubMed.
- Sus1 Modulates Chromatin Remodeling and Gene Expression via the Cell Wall Integrity Pathway in Saccharomyces cerevisiae.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- Mutant huntingtin impairs neurodevelopment in human brain organoids through CHCHD2-mediated neurometabolic failure.Nature communications · 2024Article
- Autophagy in Spinocerebellar Ataxia Type 3: From Pathogenesis to Therapeutics.International journal of molecular sciences · 2023Review
- Deubiquitinases in Neurodegeneration.Cells · 2022Review
- The Molecular Basis of Spinocerebellar Ataxia Type 7.Frontiers in neuroscience · 2022Review
- New Perspectives of Gene Therapy on Polyglutamine Spinocerebellar Ataxias: From Molecular Targets to Novel Nanovectors.Pharmaceutics · 2021Review
- An insight into structural plasticity and conformational transitions of transcriptional co-activator Sus1.PloS one · 2020Article
- Article
- Golgi Complex Dynamics and Its Implication in Prevalent Neurological Disorders.Frontiers in cell and developmental biology · 2019Review
- Planar cell polarity geneEMBO reports · 2018Article
- Comparison of spinocerebellar ataxia type 3 mouse models identifies early gain-of-function, cell-autonomous transcriptional changes in oligodendrocytes.Human molecular genetics · 2017Article
- Candida albicans Is Resistant to Polyglutamine Aggregation and Toxicity.G3 (Bethesda, Md.) · 2017Article
- Article
- Commonalities in Biological Pathways, Genetics, and Cellular Mechanism between Alzheimer Disease and Other Neurodegenerative Diseases: An In Silico-Updated Overview.Current Alzheimer research · 2017Review
- Selfish DNA and Epigenetic Repression Revisited.Genetics · 2016Article
- Real-time imaging of Huntingtin aggregates diverting target search and gene transcription.eLife · 2016Article
- Impaired muscle uptake of creatine in spinal and bulbar muscular atrophy.Annals of clinical and translational neurology · 2016Article
- An Intrabody Drug (rAAV6-INT41) Reduces the Binding of N-Terminal Huntingtin Fragment(s) to DNA to Basal Levels in PC12 Cells and Delays Cognitive Loss in the R6/2 Animal Model.Journal of neurodegenerative diseases · 2016Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Nine genetic diseases arise from expansion of CAG repeats in seemingly unrelated genes. They are referred to as polyglutamine (polyQ) diseases due to the presence of elongated glutamine tracts in the corresponding proteins. The pathologic consequences of polyQ expansion include progressive spinal, cerebellar, and neural degeneration. These pathologies are not identical, however, suggesting that disruption of protein-specific functions is crucial to establish and maintain each disease. A closer examination of protein function reveals that several act as regulators of gene expression. Here we examine the roles these proteins play in regulating gene expression, discuss how polyQ expansion may disrupt these functions to cause disease, and speculate on the neural specificity of perturbing ubiquitous gene regulators.
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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.