ArticleHuman molecular genetics2018
The long non-coding RNA NEAT1 is elevated in polyglutamine repeat expansion diseases and protects from disease gene-dependent toxicities.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- MeCP2 NID interaction with RNA: implications for Rett syndrome-relevant protein regulation.Human molecular genetics · 2026Article
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
- LncRNA-GPHN Regulates Epilepsy by Inhibiting Apoptosis via the miR-320/YWHAH Axis in an Immature Rat Model of Status Epilepticus.Journal of cellular and molecular medicine · 2025Article
- Distinct expression of NEAT1 isoforms in Parkinson's disease models suggests different roles of the variants during the disease course.Scientific reports · 2025Article
- NEAT1-mediated regulation of proteostasis and mRNA localization impacts autophagy dysregulation in Rett syndrome.Nucleic acids research · 2025Article
- RNA Immunoprecipitation (RIP) from Purified Nuclei in Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- RettDb: the Rett syndrome omics database to navigate the Rett syndrome genomic landscape.Database : the journal of biological databases and curation · 2024Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Huntingtin is an RNA binding protein and participates inScience advances · 2024Article
- Review
- Integrative modeling of lncRNA-chromatin interaction maps reveals diverse mechanisms of nuclear retention.BMC genomics · 2023Article
- Roles of lncRNAs in brain development and pathogenesis: Emerging therapeutic opportunities.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- The Emerging Role of Autophagy-Associated lncRNAs in the Pathogenesis of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Single-nuclei transcriptome analysis of Huntington disease iPSC and mouse astrocytes implicates maturation and functional deficits.iScience · 2023Article
- Non-coding RNAs in human health and disease: potential function as biomarkers and therapeutic targets.Functional & integrative genomics · 2023Review
- Long Intergenic Noncoding RNAs Affect Biological Pathways Underlying Autoimmune and Neurodegenerative Disorders.Molecular neurobiology · 2022Review
- Analysis of the circRNA and T-UCR populations identifies convergent pathways in mouse and human models of Rett syndrome.Molecular therapy. Nucleic acids · 2022Article
- The emerging role of long non-coding RNAs, microRNAs, and an accelerated epigenetic age in Huntington's disease.Frontiers in aging neuroscience · 2022Review
- Roles of Long Non-coding RNAs in the Development of Aging-Related Neurodegenerative Diseases.Frontiers in molecular neuroscience · 2022Review
- Mutant huntingtin messenger RNA forms neuronal nuclear clusters in rodent and human brains.Brain communications · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Polyglutamine (polyQ) repeat diseases are a class of neurodegenerative disorders caused by CAG-repeat expansion. There are diverse cellular mechanisms behind the pathogenesis of polyQ disorders, including transcriptional dysregulation. Interestingly, we find that levels of the long isoform of nuclear paraspeckle assembly transcript 1 (Neat1L) are elevated in the brains of mouse models of spinocerebellar ataxia types 1, 2, 7 and Huntington's disease (HD). Neat1L was also elevated in differentiated striatal neurons derived from HD knock-in mice and in HD patient brains. The elevation was mutant Huntingtin (mHTT) dependent, as knockdown of mHTT in vitro and in vivo restored Neat1L to normal levels. In additional studies, we found that Neat1L is repressed by methyl CpG binding protein 2 (MeCP2) by RNA-protein interaction but not by occupancy of MeCP2 at its promoter. We also found that NEAT1L overexpression protects from mHTT-induced cytotoxicity, while reducing it enhanced mHTT-dependent toxicity. Gene set enrichment analysis of previously published RNA sequencing data from mouse embryonic fibroblasts and cells derived from HD patients shows that loss of NEAT1L impairs multiple cellular functions, including pathways involved in cell proliferation and development. Intriguingly, the genes dysregulated in HD human brain samples overlap with pathways affected by a reduction in NEAT1, confirming the correlation of NEAT1L and HD-induced perturbations. Cumulatively, the role of NEAT1L in polyQ disease model systems and human tissues suggests that it may play a protective role in CAG-repeat expansion diseases.
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