ReviewThe Journal of biological chemistry2009
Animal models of polyglutamine diseases and therapeutic approaches.
Review in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Core biological principles and tools stemming from basic Arabidopsis research.The Plant cell · 2025Review
- Evolutionary perspective of the CAG/CAA interplay coding for pure polyglutamine stretches in proteins.NAR genomics and bioinformatics · 2025Article
- Role of Nanomedicine-Based Therapeutics in the Treatment of CNS Disorders.Molecules (Basel, Switzerland) · 2023Review
- Metabolism in Huntington's disease: a major contributor to pathology.Metabolic brain disease · 2022Review
- Small-molecule modulators of TRMT2A decrease PolyQ aggregation and PolyQ-induced cell death.Computational and structural biotechnology journal · 2022Article
- Unexpected cell type-dependent effects of autophagy on polyglutamine aggregation revealed by natural genetic variation in C. elegans.BMC biology · 2020Article
- Studying polyglutamine aggregation in Caenorhabditis elegans using an analytical ultracentrifuge equipped with fluorescence detection.Protein science : a publication of the Protein Society · 2016Article
- The Social Amoeba Dictyostelium discoideum Is Highly Resistant to Polyglutamine Aggregation.The Journal of biological chemistry · 2015Article
- An understanding of spinocerebellar ataxia.The Indian journal of medical research · 2015Article
- Neural Differentiation of Human Pluripotent Stem Cells for Nontherapeutic Applications: Toxicology, Pharmacology, and In Vitro Disease Modeling.Stem cells international · 2015Review
- Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease.Neurobiology of disease · 2012Article
- Neuronal store-operated calcium entry pathway as a novel therapeutic target for Huntington's disease treatment.Chemistry & biology · 2011Article
- Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models.Journal of genetics · 2010Review
- The rise and fall of Dimebon.Drug news & perspectives · 2010Article
- Focal nature of neurological disorders necessitates isotype-selective histone deacetylase (HDAC) inhibitors.Molecular neurobiology · 2009Review
- Alteration in memory cognition due to activation of caveolin-1 and oxidative damage in a model of dementia of Alzheimer's type.Indian journal of pharmacologyArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The dominant gain-of-function polyglutamine repeat diseases, in which the initiating mutation is known, allow development of models that recapitulate many aspects of human disease. To the extent that pathology is a consequence of disrupted fundamental cellular activities, one can effectively study strategies to ameliorate or protect against these cellular insults. Model organisms allow one to identify pathways that affect disease onset and progression, to test and screen for pharmacological agents that affect pathogenic processes, and to validate potential targets genetically as well as pharmacologically. Here, we describe polyglutamine repeat diseases that have been modeled in a variety of organisms, including worms, flies, mice, and non-human primates, and discuss examples of how they have broadened the therapeutic landscape.
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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.