ArticleThe Journal of biological chemistry2009
The smooth muscle cell-restricted KCNMB1 ion channel subunit is a direct transcriptional target of serum response factor and myocardin.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 77 citations in OpenAlex.
- Ionic regulation of cancer cell stiffness and metastatic colonization via the MRTFA-KCNMB1 axis.Developmental cell · 2026Article
- Ionic Regulation of Mechanosurveillance and Metastasis via the MRTFA/KCNMB1 Axis.bioRxiv : the preprint server for biology · 2026Article
- MAPK14 converges on key transcriptional machinery to promote vascular smooth muscle cell degeneration in abdominal aortic aneurysm.Signal transduction and targeted therapy · 2026Article
- Genetic silencing of KChannels (Austin, Tex.) · 2025Article
- Leiomodin 1 haploinsufficiency promotes smooth muscle cell proliferation and increases neointimal lesion size.Vascular pharmacology · 2025Article
- New insights into the pharmacological inhibition of SRF activity: Key inhibitory targets and mechanisms.Vascular pharmacology · 2024Review
- Article
- Recent advances in serum response factor posttranslational modifications and their therapeutic potential in cardiovascular and neurological diseases.Vascular pharmacology · 2024Review
- Suppression of smooth muscle cell inflammation by myocardin-related transcription factors involves inactivation of TANK-binding kinase 1.Scientific reports · 2024Article
- Influence of DNA Methylation on Vascular Smooth Muscle Cell Phenotypic Switching.International journal of molecular sciences · 2024Review
- Large-conductance CaFrontiers in cardiovascular medicine · 2022Article
- KArtery research · 2021Article
- Regucalcin promotes dormancy of prostate cancer.Oncogene · 2021Article
- Reorganization of Metabolism during Cardiomyogenesis Implies Time-Specific Signaling Pathway Regulation.International journal of molecular sciences · 2021Article
- Regulation of the Muscarinic MFrontiers in physiology · 2021Article
- Targeting smooth muscle cell phenotypic switching in vascular disease.JVS-vascular science · 2021Review
- Integrated analysis of lncRNAs and mRNAs reveals key trans-target genes associated with ETEC-F4ac adhesion phenotype in porcine small intestine epithelial cells.BMC genomics · 2020Article
- Induced osteogenic differentiation of human smooth muscle cells as a model of vascular calcification.Scientific reports · 2020Article
- The Role of KCNMB1 and BK Channels in Myofibroblast Differentiation and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- Transcriptional control of a novel long noncoding RNA Mymsl in smooth muscle cells by a single Cis-element and its initial functional characterization in vessels.Journal of molecular and cellular cardiology · 2020Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Large conductance calcium-activated potassium (MaxiK) channels play a pivotal role in maintaining normal arterial tone by regulating the excitation-contraction coupling process. MaxiK channels comprise alpha and beta subunits encoded by Kcnma and the cell-restricted Kcnmb genes, respectively. Although the functionality of MaxiK channel subunits has been well studied, the molecular regulation of their transcription and modulation in smooth muscle cells (SMCs) is incomplete. Using several model systems, we demonstrate down-regulation of Kcnmb1 mRNA upon SMC phenotypic modulation in vitro and in vivo. As part of a broad effort to define all functional CArG elements in the genome (i.e. the CArGome), we discovered two conserved CArG boxes located in the proximal promoter and first intron of the human KCNMB1 gene. Gel shift and chromatin immunoprecipitation assays confirmed serum response factor (SRF) binding to both CArG elements. A luciferase assay showed myocardin (MYOCD)-mediated transactivation of the KCNMB1 promoter in a CArG element-dependent manner. In vivo analysis of the human KCNMB1 promoter disclosed activity in embryonic heart and aortic SMCs; mutation of both conserved CArG elements completely abolished in vivo promoter activity. Forced expression of MYOCD increased Kcnmb1 expression in a variety of rodent and human non-SMC lines with no effect on expression of the Kcnma1 subunit. Conversely, knockdown of Srf resulted in decreases of endogenous Kcnmb1. Functional studies demonstrated MYOCD-induced, iberiotoxin-sensitive potassium currents in porcine coronary SMCs. These results reveal the first ion channel subunit as a direct target of SRF-MYOCD transactivation, providing further insight into the role of MYOCD as a master regulator of the SMC contractile phenotype.
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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.