ArticleCellular and molecular neurobiology2023
Inhibition of the Proteasome Regulator PA28 Aggravates Oxidized Protein Overload in the Diabetic Rat Brain.
Article in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Integrated Time-Series Biochemical, Transcriptomic and Metabolomic Analyses Reveal Key Pathways and Concentration-Dependent Transitions in Chironomid Larvae (Animals : an open access journal from MDPI · 2026Article
- Arsenic Inhibits the PA28α/β-PSMB5 Pathway Blocking Phosphorylated TFEB Degradation and Causing Lysosomal Dysfunction that Damages the Liver.Biological trace element research · 2026Article
- APOE4 disrupts the central dogma by arresting neuronal proteome dynamics.bioRxiv : the preprint server for biology · 2026Article
- Review
- Understanding neurodevelopmental proteasomopathies as new rare disease entities: A review of current concepts, molecular biomarkers, and perspectives.Genes & diseases · 2024Review
- Structure, Function, and Allosteric Regulation of the 20S Proteasome by the 11S/PA28 Family of Proteasome Activators.Biomolecules · 2023Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Oxidized protein overloading caused by diabetes is one accelerating pathological pathway in diabetic encephalopathy development. To determine whether the PA28-regulated function of the proteasome plays a role in diabetes-induced oxidative damaged protein degradation, brain PA28α and PA28β interference experiments were performed in a high-fat diet (HFD) and streptozotocin (STZ)-induced rat model. The present results showed that proteasome activity was changed in the brains of diabetic rats, but the constitutive subunits were not. In vivo PA28α and PA28β inhibition via adeno-associated virus (AAV) shRNA infection successfully decreased PA28 protein levels and further exacerbated oxidized proteins load by regulating proteasome catalytic activity. These findings suggest that the proteasome plays a role in the elimination of oxidized proteins and that PA28 is functionally involved in the regulation of proteasome activity in vivo. This study suggests that abnormal protein turbulence occurring in the diabetic brain could be explained by the proteasome-mediated degradation pathway. Changes in proteasome activity regulator PA28 could be a reason to induce oxidative aggregation in diabetic brain. Proteasome regulator PA28 inhibition in vivo by AAV vector injection could aggravate oxidized proteins abundance in brain of HFD-STZ diabetic rat model.
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