ArticleCell death & disease2013
Suppression of polyglutamine protein toxicity by co-expression of a heat-shock protein 40 and a heat-shock protein 110.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
- Chaperone-mediated remodelling of mutant huntingtin.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- ATP modulates holdase activity of fungal and human 110-kilodalton heat shock proteins to promote protein folding.Protein science : a publication of the Protein Society · 2026Article
- The Hsp40 cochaperone DNAJC7 regulates polyglutamine aggregation and exhibits context-dependent effects on polyglycine aggregation.The Journal of biological chemistry · 2026Article
- Phosphorylation of α‑Synuclein Fibrils at S129 Changes DNAJB1 Binding as Probed by Solid-State NMR.JACS Au · 2026Article
- GABAergic neuronal dysfunction underlies tremor in spinocerebellar ataxia 3.Disease models & mechanisms · 2025Article
- HSP110 is a modulator of amyloid beta (Aβ) aggregation and proteotoxicity.Journal of neurochemistry · 2025Article
- The Role of Heat Shock Protein 70 (HSP70) in the Pathogenesis of Ocular Diseases-Current Literature Review.Journal of clinical medicine · 2024Review
- A multi-layered network model identifies Akt1 as a common modulator of neurodegeneration.Molecular systems biology · 2023Article
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Clearance of variant Creutzfeldt-Jakob disease prions in vivo by the Hsp70 disaggregase system.Brain : a journal of neurology · 2022Article
- Cooperative amyloid fibre binding and disassembly by the Hsp70 disaggregase.The EMBO journal · 2022Article
- Identification of a HTT-specific binding motif in DNAJB1 essential for suppression and disaggregation of HTT.Nature communications · 2022Article
- Hsp40 overexpression in pacemaker neurons delays circadian dysfunction in a Drosophila model of Huntington's disease.Disease models & mechanisms · 2022Article
- A New Perspective on Huntington's Disease: How a Neurological Disorder Influences the Peripheral Tissues.International journal of molecular sciences · 2022Review
- Modifier pathways in polyglutamine (PolyQ) diseases: from genetic screens to drug targets.Cellular and molecular life sciences : CMLS · 2022Review
- Hsp40s play distinct roles during the initial stages of apolipoprotein B biogenesis.Molecular biology of the cell · 2022Article
- DNAJB11 predicts a poor prognosis and is associated with immune infiltration in thyroid carcinoma: a bioinformatics analysis.The Journal of international medical research · 2021Article
- Fluc-EGFP reporter mice reveal differential alterations of neuronal proteostasis in aging and disease.The EMBO journal · 2021Article
- Impaired inhibitory GABAergic synaptic transmission and transcription studied in single neurons by Patch-seq in Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- RACK1 modulates polyglutamine-induced neurodegeneration by promoting ERK degradation in Drosophila.PLoS genetics · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
A network of heat-shock proteins mediates cellular protein homeostasis, and has a fundamental role in preventing aggregation-associated neurodegenerative diseases. In a Drosophila model of polyglutamine (polyQ) disease, the HSP40 family protein, DNAJ-1, is a superior suppressor of toxicity caused by the aggregation of polyQ containing proteins. Here, we demonstrate that one specific HSP110 protein, 70 kDa heat-shock cognate protein cb (HSC70cb), interacts physically and genetically with DNAJ-1 in vivo, and that HSC70cb is necessary for DNAJ-1 to suppress polyglutamine-induced cell death in Drosophila. Expression of HSC70cb together with DNAJ-1 significantly enhanced the suppressive effects of DNAJ-1 on polyQ-induced neurodegeneration, whereas expression of HSC70cb alone did not suppress neurodegeneration in Drosophila models of either general polyQ disease or Huntington's disease. Furthermore, expression of a human HSP40, DNAJB1, together with a human HSP110, APG-1, protected cells from polyQ-induced neural degeneration in flies, whereas expression of either component alone had little effect. Our data provide a functional link between HSP40 and HSP110 in suppressing the cytotoxicity of aggregation-prone proteins, and suggest that HSP40 and HSP110 function together in protein homeostasis control.
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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.