ArticleProceedings of the National Academy of Sciences of the United States of America2003
Myocardin is a master regulator of smooth muscle gene expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 275 papers, 1 of them a synthesis that pooled it.
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Who cites it
275 citing papers in PubMed, 1 synthesis or guideline pooled it, 532 citations in OpenAlex.
- Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms.Nature genetics · 2017Pooled it
- Induction of human cardiomyocyte-like cells from fibroblasts by defined factors.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026Review
- Leiomodin 1 deficiency promotes lipid accumulation and redirects gene regulatory programs in smooth muscle cells exposed to oxidized LDL.Research square · 2026Article
- Spatial expression of myocardin protein in normal and disease states.American journal of physiology. Cell physiology · 2026Article
- Review
- Leiomodin 1 haploinsufficiency promotes smooth muscle cell proliferation and increases neointimal lesion size.Vascular pharmacology · 2025Article
- Smooth muscle cell (SMC)-Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death.Biochemistry and biophysics reports · 2025Article
- Poly(ADP-ribose) polymerase 1 orchestrates vascular smooth muscle cell homeostasis in arterial disease.Experimental & molecular medicine · 2025Article
- Obesity induces phenotypic switching of gastric smooth muscle cells through the activation of the PPARD/PDK4/ANGPTL4 pathway.Journal of biomedical science · 2025Article
- Ureter development and associated congenital anomalies.Nature reviews. Nephrology · 2025Review
- The 9p21.3 Coronary Artery Disease Risk Locus Drives Vascular Smooth Muscle Cells to an Osteochondrogenic State.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Novel Directly Reprogrammed Smooth Muscle Cells Promote Vascular Regeneration as Microvascular Mural Cells.Circulation · 2025Article
- Reprogrammed Smooth Muscle Cells for Vascular Repair: A New Path to Healing Ischemic Tissue.Circulation · 2025Article
- TTK Inhibition Alleviates Postinjury Neointimal Formation and Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Claudin 7 suppresses invasion and metastasis through repression of a smooth muscle actin program.The Journal of cell biology · 2024Article
- A Comprehensive Clinicopathologic and Molecular Reappraisal of GLI1 -altered Mesenchymal Tumors with Pooled Outcome Analysis Showing Poor Survival in GLI1 - amplified Versus GLI1- rearranged Tumors.The American journal of surgical pathology · 2024Article
- Basal ATP release signals through the P2YAtherosclerosis · 2024Article
- Comparative single-cell transcriptional and proteomic atlas of clinical-grade injectable mesenchymal source tissues.Science advances · 2024Article
- Integration of spatial and single-cell data across modalities with weakly linked features.Nature biotechnology · 2024Article
215 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Virtually all smooth muscle genes analyzed to date contain two or more essential binding sites for serum response factor (SRF) in their control regions. Because SRF is expressed in a wide range of cell types, it alone cannot account for smooth muscle-specific gene expression. We show that myocardin, a cardiac muscle- and smooth muscle-specific transcriptional coactivator of SRF, can activate smooth muscle gene expression in a variety of nonmuscle cell types via its association with SRF. Homodimerization of myocardin is required for maximal transcriptional activity and provides a mechanism for cooperative activation of smooth muscle genes by SRF-myocardin complexes bound to different SRF binding sites. These findings identify myocardin as a master regulator of smooth muscle gene expression and explain how SRF conveys smooth muscle specificity to its target genes.
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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.