ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Cellular defects and altered gene expression in PC12 cells stably expressing mutant huntingtin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 117 citations in OpenAlex.
- Assessing the Potential of NGF-Differentiated PC12 Cells as a Model for Synaptic Transmission.Molecular neurobiology · 2025Article
- The Common Cellular Events in the Neurodegenerative Diseases and the Associated Role of Endoplasmic Reticulum Stress.International journal of molecular sciences · 2022Review
- Reduced cell size, chromosomal aberration and altered proliferation rates are characteristics and confounding factors in the STHdh cell model of Huntington disease.Scientific reports · 2017Article
- Synaptic mutant huntingtin inhibits synapsin-1 phosphorylation and causes neurological symptoms.The Journal of cell biology · 2013Article
- Extensive changes in DNA methylation are associated with expression of mutant huntingtin.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Differential vulnerability of neurons in Huntington's disease: the role of cell type-specific features.Journal of neurochemistry · 2010Review
- Article
- Genetic interaction between expanded murine Hdh alleles and p53 reveal deleterious effects of p53 on Huntington's disease pathogenesis.Neurobiology of disease · 2006Article
- Flanking sequences profoundly alter polyglutamine toxicity in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Huntingtin forms toxic NH2-terminal fragment complexes that are promoted by the age-dependent decrease in proteasome activity.The Journal of cell biology · 2003Article
- Lack of huntingtin-associated protein-1 causes neuronal death resembling hypothalamic degeneration in Huntington's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- A cell-based assay for aggregation inhibitors as therapeutics of polyglutamine-repeat disease and validation in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Mutant huntingtin causes context-dependent neurodegeneration in mice with Huntington's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Huntingtin in health and disease.The Journal of clinical investigation · 2003Review
- Interaction of Huntington disease protein with transcriptional activator Sp1.Molecular and cellular biology · 2002Article
- Huntingtin aggregate-associated axonal degeneration is an early pathological event in Huntington's disease mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Modeling Huntington's disease in cells, flies, and mice.Molecular neurobiology · 2001Article
- The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Severe deficiencies in dopamine signaling in presymptomatic Huntington's disease mice.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Role of tetanus neurotoxin insensitive vesicle-associated membrane protein (TI-VAMP) in vesicular transport mediating neurite outgrowth.The Journal of cell biology · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Expanded polyglutamine tracts cause huntingtin and other proteins to accumulate and aggregate in neuronal nuclei. Whether the intranuclear aggregation or localization of a polyglutamine protein initiates cellular pathology remains controversial. We established stably transfected pheochromocytoma PC12 cells that express the N-terminal fragment of huntingtin containing 20 (20Q) or 150 (150Q) glutamine residues. The 150Q protein is predominantly present in the nuclei, whereas the 20Q protein is distributed throughout the cytoplasm. Electron microscopic examination confirmed that most of the 150Q protein is diffuse in the nucleus with very few microscopic aggregates observed. Compared with parental PC12 cells and cells expressing 20Q, cells expressing 150Q display abnormal morphology, lack normal neurite development, die more rapidly, and are more susceptible to apoptotic stimulation. The extent of these cellular defects in 150Q cells is correlated with the expression level of the 150Q protein. Differential display PCR and expression studies show that cells expressing 150Q have altered expression of multiple genes, including those that are important for neurite outgrowth. Our study suggests that mutant huntingtin in the nucleus is able to induce multiple cellular defects by interfering with gene expression even in the absence of aggregation.
Indexed as
Identifiers
10377328PMC6782329W1855026199What OpenQuestion holds
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.