ArticleJournal of molecular and cellular cardiology2014
Muscarinic 2 receptors modulate cardiac proteasome function in a protein kinase G-dependent manner.
Article 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 19 papers, 1 of them a synthesis that pooled it.
What it found
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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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Cullin Deneddylation Suppresses the Necroptotic Pathway in Cardiomyocytes.Frontiers in physiology · 2021Pooled it
- Promoting proteostasis by cAMP/PKA and cGMP/PKG.Trends in molecular medicine · 2025Review
- Genetic blockade of the activation of 26S proteasomes by PKA is well tolerated by mice at baseline.American journal of cardiovascular disease · 2024Article
- Inhibition of p38 Mitogen-Activated Protein Kinase Ameliorates HAP40 Depletion-Induced Toxicity and Proteasomal Defect in Huntington's Disease Model.Molecular neurobiology · 2021Article
- Mechanisms That Activate 26S Proteasomes and Enhance Protein Degradation.Biomolecules · 2021Review
- TRIB2 modulates proteasome function to reduce ubiquitin stability and protect liver cancer cells against oxidative stress.Cell death & disease · 2021Article
- CHIP phosphorylation by protein kinase G enhances protein quality control and attenuates cardiac ischemic injury.Nature communications · 2020Article
- PKG1α Cysteine-42 Redox State Controls mTORC1 Activation in Pathological Cardiac Hypertrophy.Circulation research · 2020Article
- Priming the Proteasome to Protect against Proteotoxicity.Trends in molecular medicine · 2020Review
- cGMP via PKG activates 26S proteasomes and enhances degradation of proteins, including ones that cause neurodegenerative diseases.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Targeting Protein Kinase G to Treat Cardiac Proteotoxicity.Frontiers in physiology · 2020Review
- Phosphorylation Modifications Regulating Cardiac Protein Quality Control Mechanisms.Frontiers in physiology · 2020Review
- 26S Proteasomes are rapidly activated by diverse hormones and physiological states that raise cAMP and cause Rpn6 phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Regulation of Proteasome Activity by (Post-)transcriptional Mechanisms.Frontiers in molecular biosciences · 2019Review
- Exploring the Regulation of Proteasome Function by Subunit Phosphorylation.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Regulating protein breakdown through proteasome phosphorylation.The Biochemical journal · 2017Review
- Proteasome dysfunction in cardiomyopathies.The Journal of physiology · 2017Review
- Priming the proteasome by protein kinase G: a novel cardioprotective mechanism of sildenafil.Future cardiology · 2015Review
- Autophagic-lysosomal inhibition compromises ubiquitin-proteasome system performance in a p62 dependent manner in cardiomyocytes.PloS one · 2014Article
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 1 institution in 1 country.
Funding
Abstract
Proteasome function insufficiency and inadequate protein quality control are strongly implicated in a large subset of cardiovascular disease and may play an important role in their pathogenesis. Protein degradation by the ubiquitin proteasome system can be physiologically regulated. Cardiac muscarinic 2 (M2) receptors were pharmacologically interrogated in intact mice and cultured neonatal rat ventricular myocytes (NRVMs). Proteasome-mediated proteolysis was measured with a surrogate misfolded protein, proteasome peptidase assay, and by characterizing key proteasome subunits. Successful M2 receptor manipulation in cardiomyocytes was determined by measuring an endogenous protein substrate, and in mice, the cardiovascular physiological response. M2 receptor stimulation was associated with increased proteasome-mediated proteolysis and enhanced peptidase activities, while M2 receptor inhibition yielded opposing results. Additionally, M2 receptor manipulation did not alter abundance of the key proteasome subunits, Rpt6 and β5, but significantly shifted their isoelectric points. Inhibition of protein kinase G abrogated the stimulatory effects on proteasome-mediated proteolysis from M2 receptor activation. We conclude that M2 receptor stimulation enhances, whereas M2 receptor inhibition reduces, proteasome-mediated proteolysis likely through posttranslational modifications. Protein kinase G appears to be the mediator of the M2 receptors actions.
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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.