ArticleHuman molecular genetics2015
Htt CAG repeat expansion confers pleiotropic gains of mutant huntingtin function in chromatin regulation.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Therapeutic Oligonucleotides for Neurodegenerative Diseases: Aptamer Strategies and Clay Nanoparticle-Based Delivery.Chemical record (New York, N.Y.) · 2025Review
- Neuroinflammation and the role of epigenetic-based therapies for Huntington's disease management: the new paradigm.Inflammopharmacology · 2024Review
- CAG repeat expansion in the Huntington's disease gene shapes linear and circular RNAs biogenesis.PLoS genetics · 2023Article
- Brain-Derived Neurotrophic Factor Dysregulation as an Essential Pathological Feature in Huntington's Disease: Mechanisms and Potential Therapeutics.Biomedicines · 2023Review
- Genome-wide screening in pluripotent cells identifies Mtf1 as a suppressor of mutant huntingtin toxicity.Nature communications · 2023Article
- Cerebellar granule neurons induce Cyclin D1 before the onset of motor symptoms in Huntington's disease mice.Acta neuropathologica communications · 2023Article
- Differentiation of hPSCs to Study PRC2 Role in Cell-Fate Specification and Neurodevelopment.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Truncated Analogues of a G-Quadruplex-Forming Aptamer Targeting Mutant Huntingtin: Shorter Is Better!International journal of molecular sciences · 2022Article
- Fighting the Huntington's Disease with a G-Quadruplex-Forming Aptamer Specifically Binding to Mutant Huntingtin Protein: Biophysical Characterization, In Vitro and In Vivo Studies.International journal of molecular sciences · 2022Article
- Insights into Human-Induced Pluripotent Stem Cell-Derived Astrocytes in Neurodegenerative Disorders.Biomolecules · 2022Review
- Huntington's disease iPSC models-using human patient cells to understand the pathology caused by expanded CAG repeats.Faculty reviews · 2022Review
- Epigenetic regulation in Huntington's disease.Neurochemistry international · 2021Review
- Histone Methylation Regulation in Neurodegenerative Disorders.International journal of molecular sciences · 2021Review
- Age-related and disease locus-specific mechanisms contribute to early remodelling of chromatin structure in Huntington's disease mice.Nature communications · 2021Article
- D1R- and D2R-Medium-Sized Spiny Neurons Diversity: Insights Into Striatal Vulnerability to Huntington's Disease Mutation.Frontiers in cellular neuroscience · 2021Review
- Analysis of LINE1 Retrotransposons in Huntington's Disease.Frontiers in cellular neuroscience · 2021Article
- The Polyglutamine Expansion at the N-Terminal of Huntingtin Protein Modulates the Dynamic Configuration and Phosphorylation of the C-Terminal HEAT Domain.Structure (London, England : 1993) · 2020Article
- Epigenomic Remodeling in Huntington's Disease-Master or Servant?Epigenomes · 2020Review
- DNA Methyltransferase 1 (DNMT1) Acts on Neurodegeneration by Modulating Proteostasis-Relevant Intracellular Processes.International journal of molecular sciences · 2020Article
- Chromatin accessibility and transcription dynamics during in vitro astrocyte differentiation of Huntington's Disease Monkey pluripotent stem cells.Epigenetics & chromatin · 2019Article
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
Abstract
The CAG repeat expansion in the Huntington's disease gene HTT extends a polyglutamine tract in mutant huntingtin that enhances its ability to facilitate polycomb repressive complex 2 (PRC2). To gain insight into this dominant gain of function, we mapped histone modifications genome-wide across an isogenic panel of mouse embryonic stem cell (ESC) and neuronal progenitor cell (NPC) lines, comparing the effects of Htt null and different size Htt CAG mutations. We found that Htt is required in ESC for the proper deposition of histone H3K27me3 at a subset of 'bivalent' loci but in NPC it is needed at 'bivalent' loci for both the proper maintenance and the appropriate removal of this mark. In contrast, Htt CAG size, though changing histone H3K27me3, is prominently associated with altered histone H3K4me3 at 'active' loci. The sets of ESC and NPC genes with altered histone marks delineated by the lack of huntingtin or the presence of mutant huntingtin, though distinct, are enriched in similar pathways with apoptosis specifically highlighted for the CAG mutation. Thus, the manner by which huntingtin function facilitates PRC2 may afford mutant huntingtin with multiple opportunities to impinge upon the broader machinery that orchestrates developmentally appropriate chromatin status.
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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.