ArticleThe Journal of biological chemistry2010
Modulation of myocardin function by the ubiquitin E3 ligase UBR5.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Spatial expression of myocardin protein in normal and disease states.American journal of physiology. Cell physiology · 2026Article
- E3 ubiquitin ligase UBR5 modulates circadian rhythm by facilitating the ubiquitination and degradation of the key clock transcription factor BMAL1.Acta pharmacologica Sinica · 2024Article
- SMYD2 regulates vascular smooth muscle cell phenotypic switching and intimal hyperplasia via interaction with myocardin.Cellular and molecular life sciences : CMLS · 2023Article
- SMYD2 Regulates Vascular Smooth Muscle Cell Phenotypic Switching and Intimal Hyperplasia via Interaction with Myocardin.Research square · 2023Article
- Clinicopathological Features and Prognostic Evaluation of UBR5 in Liver Cancer Patients.Pathology oncology research : POR · 2022Article
- YY1 directly interacts with myocardin to repress the triad myocardin/SRF/CArG box-mediated smooth muscle gene transcription during smooth muscle phenotypic modulation.Scientific reports · 2020Article
- Transcription factor TEAD1 is essential for vascular development by promoting vascular smooth muscle differentiation.Cell death and differentiation · 2019Article
- Differentially expressed alternatively spliced genes in skeletal muscle from cancer patients with cachexia.Journal of cachexia, sarcopenia and muscle · 2018Article
- Human Skeletal Muscle Possesses an Epigenetic Memory of Hypertrophy.Scientific reports · 2018Article
- Kelch-like Protein 21 (KLHL21) Targets IκB Kinase-β to Regulate Nuclear Factor κ-Light Chain Enhancer of Activated B Cells (NF-κB) Signaling Negatively.The Journal of biological chemistry · 2016Article
- EDD, a ubiquitin-protein ligase of the N-end rule pathway, associates with spindle assembly checkpoint components and regulates the mitotic response to nocodazole.The Journal of biological chemistry · 2015Article
- Gene coexpression networks reveal key drivers of phenotypic divergence in porcine muscle.BMC genomics · 2015Article
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
- The transcription factor TEAD1 represses smooth muscle-specific gene expression by abolishing myocardin function.The Journal of biological chemistry · 2014Article
- Microarray analysis of hepatic gene expression in juvenile Japanese flounder Paralichthys olivaceus fed diets supplemented with fish or vegetable oils.Marine biotechnology (New York, N.Y.) · 2014Article
- Structure of the HECT C-lobe of the UBR5 E3 ubiquitin ligase.Acta crystallographica. Section F, Structural biology and crystallization communications · 2012Article
- GSK3 as a Sensor Determining Cell Fate in the Brain.Frontiers in molecular neuroscience · 2012Article
- Transforming growth factor-β1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein.The Journal of biological chemistry · 2011Article
- A whole-genome RNAi screen identifies an 8q22 gene cluster that inhibits death receptor-mediated apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The N-end rule pathway and regulation by proteolysis.Protein science : a publication of the Protein Society · 2011Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Fully differentiated mature smooth muscle cells (SMCs) are characterized by the presence of a unique repertoire of smooth muscle-specific proteins. Although previous studies have shown myocardin to be a critical transcription factor for stimulating expression of smooth muscle-specific genes, the mechanisms regulating myocardin activity are still poorly understood. We used a yeast two-hybrid screen with myocardin as bait to search for factors that may regulate the transcriptional activity of the myocardin. From this screen we identified a HECT domain-containing protein UBR5 (ubiquitin protein ligase E3 component n-recognin 5) as a myocardin-binding protein. Previous studies have shown that HECT domain-containing proteins are ubiquitin E3 ligases that play an important role in protein degradation. UBR5 has, however, also been shown to regulate transcription independent of its E3 ligase activity. In the current study we demonstrated that UBR5 localized in the nuclei of SMCs and forms a complex with myocardin in vivo and in vitro. We also show that UBR5 specifically enhanced trans-activation of smooth muscle-specific promoters by the myocardin family of proteins. In addition, UBR5 significantly augmented the ability of myocardin to induce expression of endogenous SMC marker genes independent on its E3 ligase function. Conversely, depletion of endogenous UBR5 by small interfering RNA in fibroblast cells attenuated myocardin-induced smooth muscle-specific gene expression, and UBR5 knockdown in SMCs resulted in down-regulation of smooth muscle-specific genes. Furthermore, we found that UBR5 can attenuate myocardin protein degradation resulting in increased myocardin protein expression without affecting myocardin mRNA expression. The effects of UBR5 on myocardin requires only the HECT and UBR1 domains of UBR5. This study reveals an unexpected role for the ubiquitin E3 ligase UBR5 as an activator of smooth muscle differentiation through its ability to stabilize myocardin protein.
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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.