ReviewJournal of molecular and cellular cardiology2014
Regulation of cardiac proteasomes by ubiquitination, SUMOylation, and beyond.
Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 89 citations in OpenAlex.
- Gain and loss of the centrosomal protein taxilin-beta influences cardiac proteostasis and stress.Journal of molecular and cellular cardiology · 2025Article
- Solo or in Concert: SUMOylation in Pathogenic Fungi.The plant pathology journal · 2025Review
- E3 ubiquitin ligase COP1-mediated CEBPB ubiquitination regulates the inflammatory response of macrophages in sepsis-induced myocardial injury.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Genetic blockade of the activation of 26S proteasomes by PKA is well tolerated by mice at baseline.American journal of cardiovascular disease · 2024Article
- ATF3 in atherosclerosis: a controversial transcription factor.Journal of molecular medicine (Berlin, Germany) · 2022Review
- ProteinMetabolites · 2022Review
- T-Type Calcium Channels: A Mixed Blessing.International journal of molecular sciences · 2022Review
- Review
- Article
- Potential of histone deacetylase inhibitors in the control and regulation of prostate, breast and ovarian cancer.Frontiers in chemistry · 2022Review
- Role of Posttranslational Modifications of Proteins in Cardiovascular Disease.Oxidative medicine and cellular longevity · 2022Review
- Structure, Dynamics and Function of the 26S Proteasome.Sub-cellular biochemistry · 2021Review
- Proteasome Biology: Chemistry and Bioengineering Insights.Polymers · 2020Review
- Priming the Proteasome to Protect against Proteotoxicity.Trends in molecular medicine · 2020Review
- Role of WW domain E3 ubiquitin protein ligase 2 in modulating ubiquitination and Degradation of Septin4 in oxidative stress endothelial injury.Redox biology · 2020Article
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- Cellular Responses to Proteasome Inhibition: Molecular Mechanisms and Beyond.International journal of molecular sciences · 2019Review
- Specific Modification of Aged Proteasomes Revealed by Tag-Exchangeable Knock-In Mice.Molecular and cellular biology · 2019Article
- Dynamic Regulation of the 26S Proteasome: From Synthesis to Degradation.Frontiers in molecular biosciences · 2019Review
- Cardiovascular adverse events in multiple myeloma patients.Journal of thoracic disease · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The ubiquitin-proteasome system (UPS) is the major intracellular degradation system, and its proper function is critical to the health and function of cardiac cells. Alterations in cardiac proteasomes have been linked to several pathological phenotypes, including cardiomyopathies, ischemia-reperfusion injury, heart failure, and hypertrophy. Defects in proteasome-dependent cellular protein homeostasis can be causal for the initiation and progression of certain cardiovascular diseases. Emerging evidence suggests that the UPS can specifically target proteins that govern pathological signaling pathways for degradation, thus altering downstream effectors and disease outcomes. Alterations in UPS-substrate interactions in disease occur, in part, due to direct modifications of 19S, 11S or 20S proteasome subunits. Post-translational modifications (PTMs) are one facet of this proteasomal regulation, with over 400 known phosphorylation sites, over 500 ubiquitination sites and 83 internal lysine acetylation sites, as well as multiple sites for caspase cleavage, glycosylation (such as O-GlcNAc modification), methylation, nitrosylation, oxidation, and SUMOylation. Changes in cardiac proteasome PTMs, which occur in ischemia and cardiomyopathies, are associated with changes in proteasome activity and proteasome assembly; however several features of this regulation remain to be explored. In this review, we focus on how some of the less common PTMs affect proteasome function and alter cellular protein homeostasis. This article is part of a Special Issue entitled "Protein Quality Control, the Ubiquitin Proteasome System, and Autophagy".
Indexed as
Identifiers
What OpenQuestion holds
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.