ArticleMolecular and cellular biology2003
Myocardin is a critical serum response factor cofactor in the transcriptional program regulating smooth muscle cell differentiation.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.
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Who cites it
166 citing papers in PubMed, 358 citations in OpenAlex.
- Spatial expression of myocardin protein in normal and disease states.American journal of physiology. Cell physiology · 2026Article
- The Complex Role of Methylation in Regulating Vascular Smooth Muscle Cell Phenotypic States in Vascular Remodeling and Atherosclerosis.Biomolecules · 2026Review
- Leiomodin 1 haploinsufficiency promotes smooth muscle cell proliferation and increases neointimal lesion size.Vascular pharmacology · 2025Article
- Fibronectin-dependent integrin signaling drives EphA2 expression in vascular smooth muscle cells.American journal of physiology. Cell physiology · 2025Article
- The myometrial transcriptome changes in mares with endometrosis.Scientific reports · 2025Article
- Hippo in smooth muscle - a therapeutic target in vascular diseases driven by aging and hypertension.Frontiers in physiology · 2025Review
- Suppression of smooth muscle cell inflammation by myocardin-related transcription factors involves inactivation of TANK-binding kinase 1.Scientific reports · 2024Article
- Developing Novel Genomic Risk Stratification Models in Soft Tissue and Uterine Leiomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- The Future of Targeted Therapy for Leiomyosarcoma.Cancers · 2024Review
- Epigenetic regulation of vascular smooth muscle cell phenotypic switch and neointimal formation by PRMT5.Cardiovascular research · 2023Article
- The role of Gata3 in renin cell identity.American journal of physiology. Renal physiology · 2023Article
- Analysis of Cre lines for targeting embryonic airway smooth muscle.Developmental biology · 2023Article
- Plasticity in airway smooth muscle differentiation during mouse lung development.Developmental cell · 2023Article
- Actin-related protein 5 suppresses the cooperative activation of cardiac gene transcription by myocardin and MEF2.FEBS open bio · 2023Article
- LRP1 protects against excessive superior mesenteric artery remodeling by modulating angiotensin II-mediated signaling.JCI insight · 2023Article
- Single-nucleus chromatin accessibility profiling highlights regulatory mechanisms of coronary artery disease risk.Nature genetics · 2022Article
- YAP and TAZ in Vascular Smooth Muscle Confer Protection Against Hypertensive Vasculopathy.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Anemoside B4 Inhibits Vascular Smooth Muscle Cell Proliferation, Migration, and Neointimal Hyperplasia.Frontiers in cardiovascular medicine · 2022Article
- H3K4 di-methylation governs smooth muscle lineage identity and promotes vascular homeostasis by restraining plasticity.Developmental cell · 2021Article
- Serum response factor-cofactor interactions and their implications in disease.The FEBS journal · 2021Review
106 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The SAP family transcription factor myocardin functionally synergizes with serum response factor (SRF) and plays an important role in cardiac development. To determine the function of myocardin in the smooth muscle cell (SMC) lineage, we mapped the pattern of myocardin gene expression and examined the molecular mechanisms underlying transcriptional activity of myocardin in SMCs and embryonic stem (ES) cells. The human and murine myocardin genes were expressed in vascular and visceral SMCs at levels equivalent to or exceeding those observed in the heart. During embryonic development, the myocardin gene was expressed abundantly in a precise, developmentally regulated pattern in SMCs. Forced expression of myocardin transactivated multiple SMC-specific transcriptional regulatory elements in non-SMCs. By contrast, myocardin-induced transactivation was not observed in SRF(-/-) ES cells but could be rescued by forced expression of SRF or the SRF DNA-binding domain. Furthermore, expression of a dominant-negative myocardin mutant protein or small-interfering-RNA-induced myocardin knockdown significantly reduced SM22 alpha promoter activity in SMCs. Most importantly, forced expression of myocardin activated expression of the SM22 alpha, smooth muscle alpha-actin, and calponin-h1 genes in undifferentiated mouse ES cells. Taken together, these data demonstrate that myocardin plays an important role in the SRF-dependent transcriptional program that regulates SMC development and differentiation.
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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.