ArticleMolecular and cellular biology1997
Myocyte-specific enhancer factor 2 and thyroid hormone receptor associate and synergistically activate the alpha-cardiac myosin heavy-chain gene.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 91 citations in OpenAlex.
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- OCT4 induces long-lived dedifferentiated kidney progenitors poised to redifferentiate in 3D kidney spheroids.Molecular therapy. Methods & clinical development · 2023Article
- Protective Effects of Thyroid Hormone Deprivation on Progression of Maladaptive Cardiac Hypertrophy and Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- cAMP induces hypertrophy and alters DNA methylation in HL-1 cardiomyocytes.American journal of physiology. Cell physiology · 2015Article
- Caffeine exposure alters cardiac gene expression in embryonic cardiomyocytes.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- THRAP3 interacts with HELZ2 and plays a novel role in adipocyte differentiation.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Mef2c regulates transcription of the extracellular matrix protein cartilage link protein 1 in the developing murine heart.PloS one · 2013Article
- Promoter analysis of ventricular myosin heavy chain (vmhc) in zebrafish embryos.Developmental dynamics : an official publication of the American Association of Anatomists · 2009Article
- Transient and transgenic analysis of the zebrafish ventricular myosin heavy chain (vmhc) promoter: an inhibitory mechanism of ventricle-specific gene expression.Developmental dynamics : an official publication of the American Association of Anatomists · 2009Article
- Physical interaction between TBX5 and MEF2C is required for early heart development.Molecular and cellular biology · 2009Article
- Cardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Cooperation between MEF2 and PPARgamma in human intestinal beta,beta-carotene 15,15'-monooxygenase gene expression.BMC molecular biology · 2006Article
- Phosphorylation-facilitated sumoylation of MEF2C negatively regulates its transcriptional activity.BMC biochemistry · 2006Article
- Thyroid hormone induces cardiac myocyte hypertrophy in a thyroid hormone receptor alpha1-specific manner that requires TAK1 and p38 mitogen-activated protein kinase.Molecular endocrinology (Baltimore, Md.) · 2005Article
- Jumonji represses atrial natriuretic factor gene expression by inhibiting transcriptional activities of cardiac transcription factors.Molecular and cellular biology · 2004Article
- Phosphorylation and alternative pre-mRNA splicing converge to regulate myocyte enhancer factor 2C activity.Molecular and cellular biology · 2004Article
- Functional interaction between peroxisome proliferator-activated receptors-alpha and Mef-2C on human carnitine palmitoyltransferase 1beta (CPT1beta) gene activation.Nucleic acids research · 2004Article
- p300/cAMP-response-element-binding-protein ('CREB')-binding protein (CBP) modulates co-operation between myocyte enhancer factor 2A (MEF2A) and thyroid hormone receptor-retinoid X receptor.The Biochemical journal · 2003Article
- Smad proteins function as co-modulators for MEF2 transcriptional regulatory proteins.Nucleic acids research · 2001Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The muscle-specific regulatory region of the alpha-cardiac myosin heavy-chain (MHC) gene contains the thyroid hormone response element (TRE) and two A/T-rich DNA sequences, designated A/T1 and A/T2, the putative myocyte-specific enhancer factor 2 (MEF2) binding sites. We investigated the roles of the TRE and MEF2 binding sites and the potential interaction between thyroid hormone receptor (TR) and MEF2 proteins regulating the alpha-MHC promoter. Deletion mutation analysis indicated that both the A/T2 motif and TRE were required for muscle-specific expression of the alpha-MHC gene. The alpha-MHC enhancer containing both the A/T2 motif and TRE was synergistically activated by coexpression of MEF2 and TR in nonmuscle cells, whereas neither factor by itself activated the alpha-MHC reporters. The reporter construct containing the A/T2 sequence and the TRE linked to a heterologous promoter also showed synergistic activation by coexpression of MEF2 and TR in nonmuscle cells. Moreover, protein binding assays demonstrated that MEF2 and TR specifically bound to one another in vitro and in vivo. The MADS domain of MEF2 and the DNA-binding domain of TR were necessary and sufficient to mediate their physical interaction. Our results suggest that the members of the MADS family (MEF2) and steroid receptor superfamily (TR) interact with one another to synergistically activate the alpha-cardiac MHC gene expression.
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