ArticleAntioxidants & redox signaling2014
Protective role of DNJ-27/ERdj5 in Caenorhabditis elegans models of human neurodegenerative diseases.
Article in Antioxidants & redox signaling, 2014. 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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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- A Brief Review on Caenorhabditis elegans Role in Modelling Neurodegenerative Disease.Central nervous system agents in medicinal chemistry · 2025Review
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- Decreased Hsp90 activity protects against TDP-43 neurotoxicity in a C. elegans model of amyotrophic lateral sclerosis.PLoS genetics · 2024Article
- Endoplasmic reticulum unfolded protein response transcriptional targets of XBP-1s mediate rescue from tauopathy.Communications biology · 2024Article
- NOVA1 prevents overactivation of the unfolded protein response and facilitates chromatin access during human white adipogenesis.Nucleic acids research · 2023Article
- ERdj5 protects goblet cells from endoplasmic reticulum stress-mediated apoptosis under inflammatory conditions.Experimental & molecular medicine · 2023Article
- Mn(II) Quinoline Complex (4QMn) Restores Proteostasis and Reduces Toxicity in Experimental Models of Huntington's Disease.International journal of molecular sciences · 2022Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
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- Thioredoxin-80 protects against amyloid-beta pathology through autophagic-lysosomal pathway regulation.Molecular psychiatry · 2021Article
- The conserved transmembrane protein TMEM-39 coordinates with COPII to promote collagen secretion and regulate ER stress response.PLoS genetics · 2021Article
- The Mitochondrial PHB Complex Determines Lipid Composition and Interacts With the Endoplasmic Reticulum to Regulate Ageing.Frontiers in physiology · 2021Article
- Article
- Synergistic activation of AMPK prevents from polyglutamine-induced toxicity in Caenorhabditis elegans.Pharmacological research · 2020Article
- Inhibition of α-Synuclein Aggregation and Mature Fibril Disassembling With a Minimalistic Compound, ZPDm.Frontiers in bioengineering and biotechnology · 2020Article
- The glutathione system and the related thiol network in Caenorhabditis elegans.Redox biology · 2019Review
- ApoE-associated modulation of neuroprotection from Aβ-mediated neurodegeneration in transgenicDisease models & mechanisms · 2019Article
- Pasteurized Orange Juice Rich in Carotenoids ProtectsOxidative medicine and cellular longevity · 2019Article
- ZPD-2, a Small Compound That Inhibits α-Synuclein Amyloid Aggregation and Its Seeded Polymerization.Frontiers in molecular neuroscience · 2019Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
aimsCells have developed quality control systems for protection against proteotoxicity. Misfolded and aggregation-prone proteins, which are behind the initiation and progression of many neurodegenerative diseases (ND), are known to challenge the proteostasis network of the cells. We aimed to explore the role of DNJ-27/ERdj5, an endoplasmic reticulum (ER)-resident thioredoxin protein required as a disulfide reductase for the degradation of misfolded proteins, in well-established Caenorhabditis elegans models of Alzheimer, Parkinson and Huntington diseases.
resultsWe demonstrate that DNJ-27 is an ER luminal protein and that its expression is induced upon ER stress via IRE-1/XBP-1. When dnj-27 expression is downregulated by RNA interference we find an increase in the aggregation and associated pathological phenotypes (paralysis and motility impairment) caused by human β-amyloid peptide (Aβ), α-synuclein (α-syn) and polyglutamine (polyQ) proteins. In turn, DNJ-27 overexpression ameliorates these deleterious phenotypes. Surprisingly, despite being an ER-resident protein, we show that dnj-27 downregulation alters cytoplasmic protein homeostasis and causes mitochondrial fragmentation. We further demonstrate that DNJ-27 overexpression substantially protects against the mitochondrial fragmentation caused by human Aβ and α-syn peptides in these worm models. INNOVATION: We identify C. elegans dnj-27 as a novel protective gene for the toxicity associated with the expression of human Aβ, α-syn and polyQ proteins, implying a protective role of ERdj5 in Alzheimer, Parkinson and Huntington diseases.
conclusionOur data support a scenario where the levels of DNJ-27/ERdj5 in the ER impact cytoplasmic protein homeostasis and the integrity of the mitochondrial network which might underlie its protective effects in models of proteotoxicity associated to human ND.
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