ArticleJournal of molecular endocrinology2016
MuRF1 mono-ubiquitinates TRα to inhibit T3-induced cardiac hypertrophy in vivo.
Article in Journal of molecular endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- The Role of Muscle Ring Finger-1 (MuRF1), MuRF2, MuRF3, and Atrogin-1 on Bone Microarchitecture In Vivo.Cell biochemistry and biophysics · 2022Article
- Sex impacts cardiac function and the proteome response to thyroid hormone in aged mice.Proteome science · 2020Article
- Role of Muscle-Specific Histone Methyltransferase (Smyd1) in Exercise-Induced Cardioprotection against Pathological Remodeling after Myocardial Infarction.International journal of molecular sciences · 2020Article
- Acetylation modulates thyroid hormone receptor intracellular localization and intranuclear mobility.Molecular and cellular endocrinology · 2019Article
- The role of post-translational modifications in cardiac hypertrophy.Journal of cellular and molecular medicine · 2019Review
- Muscle-specific regulation of right ventricular transcriptional responses to chronic hypoxia-induced hypertrophy by the muscle ring finger-1 (MuRF1) ubiquitin ligase in mice.BMC medical genetics · 2018Article
- Thyroid hormone receptor localization in target tissues.The Journal of endocrinology · 2018Review
- Emergence of Members of TRAF and DUB of Ubiquitin Proteasome System in the Regulation of Hypertrophic Cardiomyopathy.Frontiers in genetics · 2018Review
- Effects of the kinase inhibitor sorafenib on heart, muscle, liver and plasma metabolism in vivo using non-targeted metabolomics analysis.British journal of pharmacology · 2017Article
- Metabolic reprogramming via PPARα signaling in cardiac hypertrophy and failure: From metabolomics to epigenetics.American journal of physiology. Heart and circulatory physiology · 2017Review
- Non-Targeted Metabolomics Analysis of the Effects of Tyrosine Kinase Inhibitors Sunitinib and Erlotinib on Heart, Muscle, Liver and Serum Metabolism In Vivo.Metabolites · 2017Article
- Post-translationally modified muscle-specific ubiquitin ligases as circulating biomarkers in experimental cancer cachexia.American journal of cancer research · 2017Article
- Cardiac ubiquitin ligases: Their role in cardiac metabolism, autophagy, cardioprotection and therapeutic potential.Biochimica et biophysica acta · 2016Review
- Cessation of biomechanical stretch model of C2C12 cells models myocyte atrophy and anaplerotic changes in metabolism using non-targeted metabolomics analysis.The international journal of biochemistry & cell biology · 2016Article
- Repair Injured Heart by Regulating Cardiac Regenerative Signals.Stem cells international · 2016Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Thyroid hormone (TH) is recognized for its role in cellular metabolism and growth and participates in homeostasis of the heart. T3 activates pro-survival pathways including Akt and mTOR. Treatment with T3 after myocardial infarction is cardioprotective and promotes elements of physiological hypertrophic response after cardiac injury. Although T3 is known to benefit the heart, very little about its regulation at the molecular level has been described to date. The ubiquitin proteasome system (UPS) regulates nuclear hormone receptors such as estrogen, progesterone, androgen, and glucocorticoid receptors by both degradatory and non-degradatory mechanisms. However, how the UPS regulates T3-mediated activity is not well understood. In this study, we aim to determine the role of the muscle-specific ubiquitin ligase muscle ring finger-1 (MuRF1) in regulating T3-induced cardiomyocyte growth. An increase in MuRF1 expression inhibits T3-induced physiological cardiac hypertrophy, whereas a decrease in MuRF1 expression enhances T3's activity both in vitro and in cardiomyocytes in vivo MuRF1 interacts directly with TRα to inhibit its activity by posttranslational ubiquitination in a non-canonical manner. We then demonstrated that a nuclear localization apparatus that regulates/inhibits nuclear receptors by sequestering them within a subcompartment of the nucleus was necessary for MuRF1 to inhibit T3 activity. This work implicates a novel mechanism that enhances the beneficial T3 activity specifically within the heart, thereby offering a potential target to enhance cardiac T3 activity in an organ-specific manner.
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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.