ArticleCirculation. Heart failure2013
Impaired assembly and post-translational regulation of 26S proteasome in human end-stage heart failure.
Article in Circulation. Heart failure, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 47 citations in OpenAlex.
- Promoting proteostasis by cAMP/PKA and cGMP/PKG.Trends in molecular medicine · 2025Review
- The Ubiquitin-Proteasome System: A Key Regulatory Hub in Myocarditis Leading to Dilated Cardiomyopathy.Journal of inflammation research · 2025Review
- Integrating Clinical Phenotype With Multiomics Analyses of Human Cardiac Tissue Unveils Divergent Metabolic Remodeling in Genotype-Positive and Genotype-Negative Patients With Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2024Article
- Stress-Induced Proteasome Sub-Cellular Translocation in Cardiomyocytes Causes Altered Intracellular Calcium Handling and Arrhythmias.International journal of molecular sciences · 2024Article
- Genetic ablation of Lmp2 increases the susceptibility for impaired cardiac function.Frontiers in molecular biosciences · 2024Article
- Myostatin/AKT/FOXO Signaling Is Altered in Human Non-Ischemic Dilated Cardiomyopathy.Life (Basel, Switzerland) · 2022Article
- The 20S as a stand-alone proteasome in cells can degrade the ubiquitin tag.Nature communications · 2021Article
- Article
- Heart Failure With Targeted Cancer Therapies: Mechanisms and Cardioprotection.Circulation research · 2021Review
- Structural Insights into Substrate Recognition and Processing by the 20S Proteasome.Biomolecules · 2021Review
- Phosphorylation Modifications Regulating Cardiac Protein Quality Control Mechanisms.Frontiers in physiology · 2020Review
- KPC1 alleviates hypoxia/reoxygenation-induced apoptosis in rat cardiomyocyte cells though BAX degradation.Journal of cellular physiology · 2019Article
- Role of the COP9 Signalosome (CSN) in Cardiovascular Diseases.Biomolecules · 2019Review
- Untying the knot: protein quality control in inherited cardiomyopathies.Pflugers Archiv : European journal of physiology · 2019Review
- Highly Dynamic Changes in the Activity and Regulation of Macroautophagy in Hearts Subjected to Increased Proteotoxic Stress.Frontiers in physiology · 2019Article
- Fine-tuning the ubiquitin-proteasome system to treat pulmonary fibrosis.Connective tissue research · 2019Review
- A Cycle of Altered Proteasome and Reactive Oxygen Species Production in Renal Proximal Tubular Cells.Toxicology and forensic medicine : open journal · 2019Article
- Ubiquitin and Ubiquitin-like proteins in cardiac disease and protection.Current drug targets · 2018Review
- Proteasome dysfunction in cardiomyopathies.The Journal of physiology · 2017Review
- Metabolic Origins of Heart Failure.JACC. Basic to translational science · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThis study examined the hypothesis that 26S proteasome dysfunction in human end-stage heart failure is associated with decreased docking of the 19S regulatory particle to the 20S proteasome. Previous studies have demonstrated that 26S proteasome activity is diminished in human end-stage heart failure associated with oxidation of the 19S regulatory particle Rpt5 subunit. Docking of the 19S regulatory particle to the 20S proteasome requires functional Rpt subunit ATPase activity and phosphorylation of the α-type subunits. METHODS AND
resultsAn enriched proteasome fraction was prepared from 7 human nonfailing and 10 failing heart explants. Native gel electrophoresis assessed docking of 19S to 20S proteasome revealing 3 proteasome populations (20S, 26S, and 30S proteasomes). In failing hearts, 30S proteasomes were significantly lower (P=0.048) by 37% suggesting diminished docking. Mass spectrometry-based phosphopeptide analysis demonstrated that the relative ratio of phosphorylated:non phosphorylated α7 subunit (serine250) of the 20S proteasome was significantly less (P=0.011) by almost 80% in failing hearts. Rpt ATPase activity was determined in the enriched fraction and after immunoprecipitation with an Rpt6 antibody. ATPase activity (ρmol PO4/μg protein per hour) of the total fraction was lowered from 291±97 to 194±27 and in the immunoprecipitated fraction from 42±12 to 3±2 (P=0.005) in failing hearts.
conclusionsThese studies suggest that diminished 26S activity in failing human hearts may be related to impaired docking of the 19S to the 20S as a result of decreased Rpt subunit ATPase activity and α7 subunit phosphorylation.
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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.