ArticleThe Journal of clinical investigation2001
CArG elements control smooth muscle subtype-specific expression of smooth muscle myosin in vivo.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
53 citing papers in PubMed, 141 citations in OpenAlex.
- TGF-β: The Molecular Mechanisms of Atherosclerosis - insights into SMAD Pathways and Gene Therapy Prospects.Current medicinal chemistry · 2026Review
- 3D confinement alters smooth muscle cell responses to chemical and mechanical cues.APL bioengineering · 2024Article
- MKL-1 suppresses ferroptosis by activating system Xc- and increasing glutathione synthesis.International journal of biological sciences · 2023Article
- Progerin mislocalizes myocardin-related transcription factor in Hutchinson-Guilford Progeria syndrome.Vascular biology (Bristol, England) · 2022Article
- Impact of Notch3 Activation on Aortic Aneurysm Development in Marfan Syndrome.Journal of immunology research · 2022Article
- Serum response factor-cofactor interactions and their implications in disease.The FEBS journal · 2021Review
- Cathelicidin Modulates Vascular Smooth Muscle Cell Phenotypic Switching through ROS/IL-6 Pathway.Antioxidants (Basel, Switzerland) · 2020Article
- Early Programming of Adult Systemic Essential Hypertension.International journal of molecular sciences · 2020Review
- Aortic "Disease-in-a-Dish": Mechanistic Insights and Drug Development Using iPSC-Based Disease Modeling.Frontiers in cell and developmental biology · 2020Review
- Epigenetics and vascular diseases.Journal of molecular and cellular cardiology · 2019Review
- An update on clonality: what smooth muscle cell type makes up the atherosclerotic plaque?F1000Research · 2018Review
- Blood pressure-associated polymorphism controls ARHGAP42 expression via serum response factor DNA binding.The Journal of clinical investigation · 2017Article
- Set7 mediated interactions regulate transcriptional networks in embryonic stem cells.Nucleic acids research · 2016Article
- Noncoding RNAs in smooth muscle cell homeostasis: implications in phenotypic switch and vascular disorders.Pflugers Archiv : European journal of physiology · 2016Review
- The short and long of noncoding sequences in the control of vascular cell phenotypes.Cellular and molecular life sciences : CMLS · 2015Review
- Upregulated expression of STIM2, TRPC6, and Orai2 contributes to the transition of pulmonary arterial smooth muscle cells from a contractile to proliferative phenotype.American journal of physiology. Cell physiology · 2015Article
- Variability in vascular smooth muscle cell stretch-induced responses in 2D culture.Vascular cell · 2015Article
- DNA methylation of a GC repressor element in the smooth muscle myosin heavy chain promoter facilitates binding of the Notch-associated transcription factor, RBPJ/CSL1.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- Modulation of cysteine-rich protein 2 expression in vascular injury and atherosclerosis.Molecular biology reports · 2014Article
- Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis.Journal of biomedical research · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Expression of smooth muscle myosin heavy chain (SM-MHC) is tightly controlled depending on the differentiated state of smooth muscle cells (SMCs). To better understand the mechanisms that regulate transcription of the SM-MHC gene in vivo, we tested the function of several conserved CArG elements contained within the -4200 to +11,600 region of this gene that we had previously shown to drive SMC-specific expression in transgenic mice. CArG1 in the 5'-flanking sequence was required for all SMCs, while CArG2 and a novel intronic CArG element were differentially required in SMC subtypes. Of particular note, mutation of the intronic CArG selectively abolished expression in large arteries. A promoter construct containing three repeats of a conserved 227-bp intronic CArG-containing region was sufficient to direct transcription in vascular SMCs in transgenic mice, although this construct was also expressed in skeletal and cardiac muscle. These results support a model in which transcriptional regulation of SM-MHC is controlled by multiple positive and negative modular control regions that differ between SMCs and non-SMCs and among SMC subtypes. We also demonstrated that the CArG elements of the endogenous SM-MHC gene were bound by SRF in chromatin.
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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.