ArticleThe Journal of biological chemistry2014
NADH binds and stabilizes the 26S proteasomes independent of ATP.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Key features of the innate immune response is mediated by the immunoproteasome in microglia.Scientific reports · 2025Article
- Regulation of ubiquitin-proteasome system and its relative pathways in pancreatic adenocarcinoma.BioImpacts : BI · 2025Review
- A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression.Acta biomaterialia · 2024Article
- Dihydrolipoamide dehydrogenase (DLD) is a novel molecular target of bortezomib.Cell death & disease · 2024Article
- Mechanisms of ubiquitin-independent proteasomal degradation and their roles in age-related neurodegenerative disease.Frontiers in cell and developmental biology · 2024Review
- Ubiquitin-Dependent and Independent Proteasomal Degradation in Host-Pathogen Interactions.Molecules (Basel, Switzerland) · 2023Review
- Interplay between proteasome function and inflammatory responses in e-cig vapor condensate-challenged lung epithelial cells.Archives of toxicology · 2023Article
- Method of Monitoring 26S Proteasome in Cells Revealed the Crucial Role of PSMA3 C-Terminus in 26S Integrity.Biomolecules · 2023Article
- The protein organization of a red blood cell.Cell reports · 2022Article
- A novel role of lysophosphatidic acid (LPA) in human myeloma resistance to proteasome inhibitors.Journal of hematology & oncology · 2022Article
- Review
- Degradation of Intrinsically Disordered Proteins by the NADH 26S Proteasome.Biomolecules · 2020Article
- Cross-talk between redox signalling and protein aggregation.Biochemical Society transactions · 2020Review
- NADCell metabolism · 2019Review
- Mitochondrial metabolism promotes adaptation to proteotoxic stress.Nature chemical biology · 2019Article
- Olfaction regulates organismal proteostasis and longevity via microRNA-dependent signaling.Nature metabolism · 2019Article
- Diarylcarbonates are a new class of deubiquitinating enzyme inhibitor.Bioorganic & medicinal chemistry letters · 2019Article
- Defenses against Pro-oxidant Forces - Maintenance of Cellular and Genomic Integrity and Longevity.Radiation research · 2018Review
- Oncogenic addiction to high 26S proteasome level.Cell death & disease · 2018Article
- Proteostasis, oxidative stress and aging.Redox biology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 26S proteasome is the end point of the ubiquitin- and ATP-dependent degradation pathway. The 26S proteasome complex (26S PC) integrity and function has been shown to be highly dependent on ATP and its homolog nucleotides. We report here that the redox molecule NADH binds the 26S PC and is sufficient in maintaining 26S PC integrity even in the absence of ATP. Five of the 19S proteasome complex subunits contain a putative NADH binding motif (GxGxxG) including the AAA-ATPase subunit, Psmc1 (Rpt2). We demonstrate that recombinant Psmc1 binds NADH via the GxGxxG motif. Introducing the ΔGxGxxG Psmc1 mutant into cells results in reduced NADH-stabilized 26S proteasomes and decreased viability following redox stress induced by the mitochondrial inhibitor rotenone. The newly identified NADH binding of 26S proteasomes advances our understanding of the molecular mechanisms of protein degradation and highlights a new link between protein homeostasis and the cellular metabolic/redox state.
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Registered trials
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.