ReviewNucleus (Austin, Tex.)
Polyglutamine (polyQ) disorders: the chromatin connection.
Review in Nucleus (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Developmental and physiological impacts of pathogenic human huntingtin protein in the nervous system.Neurobiology of disease · 2024Article
- Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration.ACS chemical neuroscience · 2024Review
- Neuroprotective effects of flavonoids: endoplasmic reticulum as the target.Frontiers in neuroscience · 2024Review
- Transcriptional and Histone Acetylation Changes Associated with CRE Elements Expose Key Factors Governing the Regulatory Circuit in the Early Stage of Huntington's Disease Models.International journal of molecular sciences · 2023Article
- What the Gut Tells the Brain-Is There a Link between Microbiota and Huntington's Disease?International journal of molecular sciences · 2023Review
- Phenome-wide association study of loci harboring de novo tandem repeat mutations in UK Biobank exomes.Nature communications · 2022Article
- Fic and non-Fic AMPylases: protein AMPylation in metazoans.Open biology · 2021Article
- Epigenetic mechanisms of neurodegenerative diseases and acute brain injury.Neurochemistry international · 2020Review
- Article
- Hat1 acetylates histone H4 and modulates the transcriptional program in Drosophila embryogenesis.Scientific reports · 2019Article
- Open chromatin structure in PolyQ disease-related genes: a potential mechanism for CAG repeat expansion in the normal human population.NAR genomics and bioinformatics · 2019Article
- Tissue-Specific Upregulation of Drosophila Insulin Receptor (InR) Mitigates Poly(Q)-Mediated Neurotoxicity by Restoration of Cellular Transcription Machinery.Molecular neurobiology · 2019Article
- Roles of Post-translational Modifications in Spinocerebellar Ataxias.Frontiers in cellular neuroscience · 2018Review
- Targeted Downregulation of dMyc Suppresses Pathogenesis of Human Neuronal Tauopathies in Drosophila by Limiting Heterochromatin Relaxation and Tau Hyperphosphorylation.Molecular neurobiology · 2017Article
- A Drosophila model of Huntington disease-like 2 exhibits nuclear toxicity and distinct pathogenic mechanisms from Huntington disease.Human molecular genetics · 2016Article
- Statistical Enrichment of Epigenetic States Around Triplet Repeats that Can Undergo Expansions.Frontiers in neuroscience · 2016Article
- HDAC inhibition imparts beneficial transgenerational effects in Huntington's disease mice via altered DNA and histone methylation.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Involvement of HDAC1 and HDAC3 in the Pathology of Polyglutamine Disorders: Therapeutic Implications for Selective HDAC1/HDAC3 Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2014Article
- From pathways to targets: understanding the mechanisms behind polyglutamine disease.BioMed research international · 2014Review
- Balancing chromatin remodeling and histone modifications in transcription.Trends in genetics : TIG · 2013Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Polyglutamine (PolyQ)-related diseases are dominant late-onset genetic disorders that are manifested by progressive neurodegeneration, leading to behavioral and physical impairments. An increased body of evidence suggests that chromatin structure and epigenetic regulation are involved in disease pathology. PolyQ diseases often display an aberrant transcriptional regulation due to the disrupted function of histone-modifying complexes and altered interactions of the polyQ-extended proteins with chromatin-related factors. In this review we describe recent findings relating to the role of chromatin in polyQ diseases. We discuss the involvement of epigenetic-related factors and chromatin structure in genomic instability of CAG repeats; we describe changes in the expression and regulation of chromatin-related enzymes and in the levels and patterns of histone modifications in disease state; we illustrate the potential beneficial effects of different histone deacetylase (HDAC) inhibitors for the treatment of polyQ diseases, and we end by describing the potential use of human pluripotent stem cells and their differentiated derivatives for modeling polyQ diseases in vitro. Taken together, these accumulating studies strongly suggest that disrupted chromatin regulation may be directly involved with the pathophysiology of polyQ-related diseases.
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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.