ArticleProceedings of the National Academy of Sciences of the United States of America2007
Steroid receptor coactivator 3 is a coactivator for myocardin, the regulator of smooth muscle transcription and differentiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Steroid hormone antagonism affords vascular protection in a mouse model of vascular Ehlers-Danlos syndrome.JCI insight · 2026Article
- Hormonal influence: unraveling the impact of sex hormones on vascular smooth muscle cells.Biological research · 2024Review
- Per-ARNT-Sim (PAS) Domains in Basic Helix-Loop-Helix (bHLH)-PAS Transcription Factors and Coactivators: Structures and Mechanisms.Journal of molecular biology · 2024Review
- Ligustrazine alleviates pulmonary arterial hypertension in rats by promoting the formation of myocardin transcription complex in the nucleus of pulmonary artery smooth muscle cells.Clinical and translational science · 2023Article
- Evaluation of extracellular matrix protein expression and apoptosis in the uterosacral ligaments of patients with or without pelvic organ prolapse.International urogynecology journal · 2021Article
- Predicting tissue-specific gene expression from whole blood transcriptome.Science advances · 2021Article
- Wound Healing-related Functions of the p160 Steroid Receptor Coactivator Family.Endocrinology · 2021Review
- Hypoxia-induced Downregulation of SRC-3 Suppresses Trophoblastic Invasion and Migration Through Inhibition of the AKT/mTOR Pathway: Implications for the Pathogenesis of Preeclampsia.Scientific reports · 2019Article
- Nexilin/NEXN controls actin polymerization in smooth muscle and is regulated by myocardin family coactivators and YAP.Scientific reports · 2018Article
- MRTF potentiates TEAD-YAP transcriptional activity causing metastasis.The EMBO journal · 2017Article
- Article
- Identification of a novel actin-dependent signal transducing module allows for the targeted degradation of GLI1.Nature communications · 2015Article
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
- The levels of RAC3 expression are up regulated by TNF in the inflammatory response.FEBS open bio · 2014Article
- Dose-dependent effects of a genistein-enriched diet in the heart of ovariectomized mice.Genes & nutrition · 2013Article
- Heavy and light roles: myosin in the morphogenesis of the heart.Cellular and molecular life sciences : CMLS · 2013Review
- Relaxin and gonadal steroid receptors in uterosacral ligaments of women with and without pelvic organ prolapse.International urogynecology journal · 2012Article
- 1,25-dihydroxyvitamin D3 treatment shrinks uterine leiomyoma tumors in the Eker rat model.Biology of reproduction · 2012Article
- Signaling mechanisms that regulate smooth muscle cell differentiation.Arteriosclerosis, thrombosis, and vascular biology · 2011Review
- Transcription factor rational design improves directed differentiation of human mesenchymal stem cells into skeletal myocytes.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal proliferation of vascular smooth muscle cells (VSMCs) constitutes a key event in atherosclerosis, neointimal hyperplasia, and the response to vascular injury. Estrogen receptor alpha (ERalpha) mediates the protective effects of estrogen in injured blood vessels and regulates ligand-dependent gene expression in vascular cells. However, the molecular mechanisms mediating ERalpha-dependent VSMC gene expression and VSMC proliferation after vascular injury are not well defined. Here, we report that the ER coactivator steroid receptor coactivator 3 (SRC3) is also a coactivator for the major VSMC transcription factor myocardin, which is required for VSMC differentiation to the nonproliferative, contractile state. The N terminus of SRC3, which contains a basic helix-loop-helix/Per-ARNT-Sim protein-protein interaction domain, binds the C-terminal activation domain of myocardin and enhances myocardin-mediated transcriptional activation of VSMC-specific, CArG-containing promoters, including the VSMC-specific genes SM22 and myosin heavy chain. Suppression of endogenous SRC3 expression by specific small interfering RNA attenuates myocardin transcriptional activation in cultured cells. The SRC3-myocardin interaction identifies a site of convergence for nuclear hormone receptor-mediated and VSMC-specific gene regulation and suggests a possible mechanism for the vascular protective effects of estrogen on vascular injury.
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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.