ArticleJournal of molecular and cellular cardiology2011
Regulation of Abro1/KIAA0157 during myocardial infarction and cell death reveals a novel cardioprotective mechanism for Lys63-specific deubiquitination.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Therapeutic Potential of the Deubiquitinase BRCC3 in Attenuating Ischemic Myocardial Injury and Ventricular Remodeling.Research (Washington, D.C.) · 2026Article
- Angiotensin-Converting Enzyme 2 Posttranslational Modifications and Implications for Hypertension and SARS-CoV-2: 2023 Lewis K. Dahl Memorial Lecture.Hypertension (Dallas, Tex. : 1979) · 2024Review
- The role of deubiquitinases in cardiac disease.Expert reviews in molecular medicine · 2024Review
- Ubiquitin-specific protease 11 Aggravates Ischemia-reperfusion-induced Cardiomyocyte Pyroptosis and Injury by Promoting TRAF3 DeubiquitinationBalkan medical journal · 2023Article
- ABRO1 arrests cardiomyocyte proliferation and myocardial repair by suppressing PSPH.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Weighted Gene Coexpression Network Analysis in Mouse Livers following Ischemia-Reperfusion and Extensive Hepatectomy.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Therapeutic Potential of Exosomes Derived From circRNA_0002113 Lacking Mesenchymal Stem Cells in Myocardial Infarction.Frontiers in cell and developmental biology · 2021Article
- Article
- Overexpression of Ubiquitin-Specific Protease 2 (USP2) in the Heart Suppressed Pressure Overload-Induced Cardiac Remodeling.Mediators of inflammation · 2020Article
- Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation.Molecular cell · 2019Article
- FAM175B promotes apoptosis by inhibiting ATF4 ubiquitination in esophageal squamous cell carcinoma.Molecular oncology · 2019Article
- ABRO1 suppresses tumourigenesis and regulates the DNA damage response by stabilizing p53.Nature communications · 2014Article
- Article
- The ubiquitin proteasome system and myocardial ischemia.American journal of physiology. Heart and circulatory physiology · 2013Review
- Ubiquitin receptors and protein quality control.Journal of molecular and cellular cardiology · 2013Review
- The expanding world of post-translational modifications.Journal of molecular and cellular cardiology · 2012Article
- Proteasome functional insufficiency in cardiac pathogenesis.American journal of physiology. Heart and circulatory physiology · 2011Review
- Loss of BRCC3 deubiquitinating enzyme leads to abnormal angiogenesis and is associated with syndromic moyamoya.American journal of human genetics · 2011Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Abro1 (also known as KIAA0157) is a scaffold protein that recruits polypeptides to assemble the BRISC (BRCC36-containing isopeptidase complex) deubiquitinating (DUB) enzyme. The four subunits of BRISC enzyme include Abro1, NBA1, BRE, and BRCC36 proteins. The DUB activity of the BRISC enzyme is exclusively directed against Lys63-linked polyubiquitin that does not have a proteolytic role but regulates protein function. In this report, we identified Abro1 as a specific interactor of THAP5, a zinc finger transcription factor that is involved in G2/M control and apoptosis. Abro1 was predominantly expressed in the heart and its protein level was regulated following experimentally induced myocardial ischemia/reperfusion (MI/R) injury. Furthermore, in patients with coronary artery disease (CAD), there was a dramatic increase in Abro1 protein level in the myocardial infarction (MI) area. Increase in Abro1 leads to a significant reduction in Lys63-linked ubiquitination of specific protein targets. Reducing the Abro1 protein level exacerbated cellular damage and cell death of cardiomyocytes due to MI/R injury. Additionally, overexpression of Abro1 in a heterologous system provided significant protection against oxidative stress-induced apoptosis. In conclusion, our results demonstrate that Abro1 protein level substantially increases in myocardial injury and coronary artery disease and this up-regulation is part of a novel cardioprotective mechanism. In addition, our data suggest a potential new link between Lys63-specific ubiquitination, its modulation by the BRISC DUB enzyme, and the development and progression of heart disease.
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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.