ArticleMolecular and cellular biology2003
Transcription enhancer factor 1 binds multiple muscle MEF2 and A/T-rich elements during fast-to-slow skeletal muscle fiber type transitions.
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 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
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- HDAC4-myogenin axis as an important marker of HD-related skeletal muscle atrophy.PLoS genetics · 2015Article
- Thyroid hormone regulates muscle fiber type conversion via miR-133a1.The Journal of cell biology · 2014Article
- Prognostic value of a nine-gene signature in glioma patients based on mRNA expression profiling.CNS neuroscience & therapeutics · 2014Article
- Essential role of TEA domain transcription factors in the negative regulation of the MYH 7 gene by thyroid hormone and its receptors.PloS one · 2014Article
- Myocyte enhancer factor 2 (MEF2) tethering to muscle selective A-kinase anchoring protein (mAKAP) is necessary for myogenic differentiation.Cellular signalling · 2012Article
- Differentiation and fiber type-specific activity of a muscle creatine kinase intronic enhancer.Skeletal muscle · 2011Article
- Article
- TEAD-1 overexpression in the mouse heart promotes an age-dependent heart dysfunction.The Journal of biological chemistry · 2010Article
- Human tyrosine hydroxylase natural genetic variation: delineation of functional transcriptional control motifs disrupted in the proximal promoter.Circulation. Cardiovascular genetics · 2010Article
- Evidence of MyomiR network regulation of beta-myosin heavy chain gene expression during skeletal muscle atrophy.Physiological genomics · 2009Article
- IGF-I activates the mouse type IIb myosin heavy chain gene.American journal of physiology. Cell physiology · 2009Article
- Overexpression of TEAD-1 in transgenic mouse striated muscles produces a slower skeletal muscle contractile phenotype.The Journal of biological chemistry · 2008Article
- Redundant roles of Tead1 and Tead2 in notochord development and the regulation of cell proliferation and survival.Molecular and cellular biology · 2008Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In adult mouse skeletal muscle, beta-myosin heavy chain (betaMyHC) gene expression is primarily restricted to slow type I fibers; however, its expression can be induced in fast type II fibers in response to a sustained increase in load-bearing work (mechanical overload [MOV]). Our previous betaMyHC transgenic and protein-DNA interaction studies have identified an A/T-rich element (betaA/T-rich -269/-258) that is required for slow muscle expression and which potentiates MOV responsiveness of a 293-bp betaMyHC promoter (beta293wt). Despite the GATA/MEF2-like homology of this element, we found binding of two unknown proteins that were antigenically distinct from GATA and MEF2 isoforms. By using the betaA/T-rich element as bait in a yeast one-hybrid screen of an MOV-plantaris cDNA library, we identified nominal transcription enhancer factor 1 (NTEF-1) as the specific betaA/T-rich binding factor. Electrophoretic mobility shift assay analysis confirmed that NTEF-1 represents the enriched binding activity obtained only when the betaA/T-rich element is reacted with MOV-plantaris nuclear extract. Moreover, we show that TEF proteins bind MEF2 elements located in the control region of a select set of muscle genes. In transient-coexpression assays using mouse C2C12 myotubes, TEF proteins transcriptionally activated a 293-bp betaMyHC promoter devoid of any muscle CAT (MCAT) sites, as well as a minimal thymidine kinase promoter-luciferase reporter gene driven by three tandem copies of the desmin MEF2 or palindromic Mt elements or four tandem betaA/T-rich elements. These novel findings suggest that in addition to exerting a regulatory effect by binding MCAT elements, TEF proteins likely contribute to regulation of skeletal, cardiac, and smooth muscle gene networks by binding select A/T-rich and MEF2 elements under basal and hypertrophic conditions.
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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.