ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
The induction levels of heat shock protein 70 differentiate the vulnerabilities to mutant huntingtin among neuronal subtypes.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 81 citations in OpenAlex.
- Elucidation of Site-Specific Ubiquitination on Chaperones in Response to Mutant Huntingtin.Cellular and molecular neurobiology · 2023Article
- Hsp40 overexpression in pacemaker neurons delays circadian dysfunction in a Drosophila model of Huntington's disease.Disease models & mechanisms · 2022Article
- Biosensors for Studying Neuronal Proteostasis.Frontiers in molecular neuroscience · 2022Review
- Praja1 ubiquitin ligase facilitates degradation of polyglutamine proteins and suppresses polyglutamine-mediated toxicity.Molecular biology of the cell · 2021Article
- Proteostasis in the Male and Female Germline: A New Outlook on the Maintenance of Reproductive Health.Frontiers in cell and developmental biology · 2021Review
- Histone Deacetylases Inhibitors in Neurodegenerative Diseases, Neuroprotection and Neuronal Differentiation.Frontiers in pharmacology · 2020Review
- Targeting the proteostasis network in Huntington's disease.Ageing research reviews · 2019Review
- Huntington's disease: the coming of age.Journal of genetics · 2018Review
- Mitochondrial Quality Control in Neurodegenerative Diseases: Focus on Parkinson's Disease and Huntington's Disease.Frontiers in neuroscience · 2018Review
- Modulation of Molecular Chaperones in Huntington's Disease and Other Polyglutamine Disorders.Molecular neurobiology · 2017Review
- The heat shock response in neurons and astroglia and its role in neurodegenerative diseases.Molecular neurodegeneration · 2017Review
- Proteostasis of Huntingtin in Health and Disease.International journal of molecular sciences · 2017Review
- Abnormal degradation of the neuronal stress-protective transcription factor HSF1 in Huntington's disease.Nature communications · 2017Article
- Ultra-Early Phase pathologies of Alzheimer's disease and other neurodegenerative diseases.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- RTP801 Is Involved in Mutant Huntingtin-Induced Cell Death.Molecular neurobiology · 2016Article
- Assessing a peptidylic inhibitor-based therapeutic approach that simultaneously suppresses polyglutamine RNA- and protein-mediated toxicities in patient cells and Drosophila.Disease models & mechanisms · 2016Article
- Transcription, epigenetics and ameliorative strategies in Huntington's Disease: a genome-wide perspective.Molecular neurobiology · 2015Review
- Molecular interaction between the chaperone Hsc70 and the N-terminal flank of huntingtin exon 1 modulates aggregation.The Journal of biological chemistry · 2015Article
- The biology of proteostasis in aging and disease.Annual review of biochemistry · 2015Review
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The reason why vulnerabilities to mutant polyglutamine (polyQ) proteins are different among neuronal subtypes is mostly unknown. In this study, we compared the gene expression profiles of three types of primary neurons expressing huntingtin (htt) or ataxin-1. We found that heat shock protein 70 (hsp70), a well known chaperone molecule protecting neurons in the polyQ pathology, was dramatically upregulated only by mutant htt and selectively in the granule cells of the cerebellum. Granule cells, which are insensitive to degeneration in the human Huntington's disease (HD) pathology, lost their resistance by suppressing hsp70 with siRNA, whereas cortical neurons, affected in human HD, gained resistance by overexpressing hsp70. This indicates that induction levels of hsp70 are a critical factor for determining vulnerabilities to mutant htt among neuronal subtypes. CAT (chloramphenicol acetyltransferase) assays showed that CBF (CCAAT box binding factor, CCAAT/enhancer binding protein zeta) activated, but p53 repressed transcription of the hsp70 gene in granule cells. Basal and mutant htt-induced expression levels of p53 were remarkably lower in granule cells than in cortical neurons, suggesting that different magnitudes of p53 are linked to distinct induction levels of hsp70. Surprisingly, however, heat shock factor 1 was not activated in granule cells by mutant htt. Collectively, different levels of hsp70 among neuronal subtypes might be involved in selective neuronal death in the HD pathology.
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