ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Generation of neuronal intranuclear inclusions by polyglutamine-GFP: analysis of inclusion clearance and toxicity as a function of polyglutamine length.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 94 citations in OpenAlex.
- Polyglutamine Repeats in Viruses.Molecular neurobiology · 2019Review
- Degenerate codon mixing for PCR-based manipulation of highly repetitive sequences.BMC research notes · 2018Article
- A network of genes connects polyglutamine toxicity to ploidy control in yeast.Nature communications · 2013Article
- Physical chemistry of polyglutamine: intriguing tales of a monotonous sequence.Journal of molecular biology · 2012Review
- Article
- Electroconvulsive shock ameliorates disease processes and extends survival in huntingtin mutant mice.Human molecular genetics · 2011Article
- Microtubule-dependent formation of the stigmoid body as a cytoplasmic inclusion distinct from pathological aggresomes.Histochemistry and cell biology · 2009Article
- Polyglutamine-expanded androgen receptor truncation fragments activate a Bax-dependent apoptotic cascade mediated by DP5/Hrk.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Cytoplasmic inclusions of Htt exon1 containing an expanded polyglutamine tract suppress execution of apoptosis in sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- The beta amyloid peptide can act as a modular aggregation domain.Neurobiology of disease · 2008Article
- Transcriptional repression and cell death induced by nuclear aggregates of non-polyglutamine protein.Neurobiology of disease · 2005Article
- Humanin attenuates apoptosis induced by DRPLA proteins with expanded polyglutamine stretches.Journal of molecular neuroscience : MN · 2005Article
- Expression of expanded polyglutamine protein induces behavioral changes in Drosophila (polyglutamine-induced changes in Drosophila).Cellular and molecular neurobiology · 2004Article
- Role of heat shock proteins during polyglutamine neurodegeneration: mechanisms and hypothesis.Journal of molecular neuroscience : MN · 2004Review
- Characterization of intracellular aggregates using fluorescently-tagged polyglutamine-expanded androgen receptor.Neurotoxicity research · 2001Article
- c-Src is required for glial cell line-derived neurotrophic factor (GDNF) family ligand-mediated neuronal survival via a phosphatidylinositol-3 kinase (PI-3K)-dependent pathway.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
- Toward an understanding of polyglutamine neurodegeneration.Brain pathology (Zurich, Switzerland) · 2000Review
- Analysis of the role of heat shock protein (Hsp) molecular chaperones in polyglutamine disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Cellular defects and altered gene expression in PC12 cells stably expressing mutant huntingtin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent evidence suggests that, in huntingtin and many other proteins, polyglutamine repeats are a toxic stimulus in neurodegenerative diseases. To investigate the mechanism by which these repeats may be toxic, we transfected primary rat cerebellar granule neurons with polyglutamine-green fluorescent protein (GFP) fusion constructs containing 19 (Q19-GFP), 35 (Q35-GFP), 56 (Q56-GFP), or 80 (Q80-GFP) glutamine residues. All constructs, except Q19-GFP, aggregated within the nuclei of transfected cells in a length- and time-dependent manner. Although Q35-GFP expression led to the development of several small aggregates per cell, these aggregates were cleared or degraded, and the cells remained viable. In contrast, Q80-GFP expression resulted in one or two large aggregates and induced cell death. Caspase activation was observed after Q80-GFP aggregation, but inhibition of caspases with Boc-aspartyl(OMe)-fluoromethylketone (BAF) only served to delay, not prevent, toxicity. In addition, aggregation and toxicity were not affected by other modulators of neuronal cell death such as genetic deletion of the proapoptotic bcl-2 family member bax or addition of the protein synthesis inhibitor cycloheximide. Lastly, nuclear condensation did not occur as part of the toxicity. These data suggest that polyglutamine-GFP expression is toxic to primary neurons but that the death is distinct from classical apoptosis.
Indexed as
Identifiers
9880591PMC6782221W1589011372What 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.