ArticleAntioxidants & redox signaling2015
The protein oxidation repair enzyme methionine sulfoxide reductase a modulates Aβ aggregation and toxicity in vivo.
Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- αACS chemical neuroscience · 2023Article
- Methionine Sulfoxide Reductases Suppress the Formation of the [Antioxidants (Basel, Switzerland) · 2023Article
- Discovery of genomic loci of the human cerebral cortex using genetically informed brain atlases.Science (New York, N.Y.) · 2022Article
- Neuroprotective Effects of Oligosaccharides in Rehmanniae Radix on TransgenicFrontiers in pharmacology · 2022Article
- Redox signaling and metabolism in Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Neuroprotective effects of a medium chain fatty acid, decanoic acid, isolated fromFrontiers in pharmacology · 2022Article
- S-methyl-L-cysteine Protects against Antimycin A-induced Mitochondrial Dysfunction in Neural Cells via Mimicking Endogenous Methionine-centered Redox Cycle.Current medical science · 2020Article
- Temporal pattern of neuronal insulin release during Caenorhabditis elegans aging: Role of redox homeostasis.Aging cell · 2019Article
- Defective protein repair under methionine sulfoxide A deletion drives autophagy and ARE-dependent gene transcription.Redox biology · 2018Article
- A conserved R type Methionine Sulfoxide Reductase reverses oxidized GrpEL1/Mge1 to regulate Hsp70 chaperone cycle.Scientific reports · 2018Article
- Dianxianning improved amyloid β-induced pathological characteristics partially through DAF-2/DAF-16 insulin like pathway in transgenic C. elegans.Scientific reports · 2017Article
- Intracellular repair of oxidation-damaged α-synuclein fails to target C-terminal modification sites.Nature communications · 2016Article
- Effect of methionine-35 oxidation on the aggregation of amyloid-β peptide.Biochemistry and biophysics reports · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTo examine the role of the enzyme methionine sulfoxide reductase A-1 (MSRA-1) in amyloid-β peptide (Aβ)-peptide aggregation and toxicity in vivo, using a Caenorhabditis elegans model of the human amyloidogenic disease inclusion body myositis.
resultsMSRA-1 specifically reduces oxidized methionines in proteins. Therefore, a deletion of the msra-1 gene was introduced into transgenic C. elegans worms that express the Aβ-peptide in muscle cells to prevent the reduction of oxidized methionines in proteins. In a constitutive transgenic Aβ strain that lacks MSRA-1, the number of amyloid aggregates decreases while the number of oligomeric Aβ species increases. These results correlate with enhanced synaptic dysfunction and mislocalization of the nicotinic acetylcholine receptor ACR-16 at the neuromuscular junction (NMJ). INNOVATION: This approach aims at modulating the oxidation of Aβ in vivo indirectly by dismantling the methionine sulfoxide repair system. The evidence presented here shows that the absence of MSRA-1 influences Aβ aggregation and aggravates locomotor behavior and NMJ dysfunction. The results suggest that therapies which boost the activity of the Msr system could have a beneficial effect in managing amyloidogenic pathologies.
conclusionThe absence of MSRA-1 modulates Aβ-peptide aggregation and increments its deleterious effects in vivo.
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