ArticleThe EMBO journal1994
An E box in the desmin promoter cooperates with the E box and MEF-2 sites of a distal enhancer to direct muscle-specific transcription.
Article in The EMBO journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 95 citations in OpenAlex.
- Molecular insights into the role of desmin intermediate filament network in chromatin landscape, cardiomyocyte differentiation, and maturation.Cell death & disease · 2025Article
- A Muscle Hybrid Promoter as a Novel Tool for Gene Therapy.Molecular therapy. Methods & clinical development · 2019Article
- Intermediate filaments in cardiomyopathy.Biophysical reviews · 2018Review
- Type III Intermediate Filaments Desmin, Glial Fibrillary Acidic Protein (GFAP), Vimentin, and Peripherin.Cold Spring Harbor perspectives in biology · 2017Review
- The LIM domain protein nTRIP6 acts as a co-repressor for the transcription factor MEF2C in myoblasts.Scientific reports · 2016Article
- Desmin enters the nucleus of cardiac stem cells and modulates Nkx2.5 expression by participating in transcription factor complexes that interact with the nkx2.5 gene.Biology open · 2016Article
- Desmin related disease: a matter of cell survival failure.Current opinion in cell biology · 2015Review
- Muscle structure influences utrophin expression in mdx mice.PLoS genetics · 2014Article
- Sequential association of myogenic regulatory factors and E proteins at muscle-specific genes.Skeletal muscle · 2011Article
- ChIPing the cistrome of PXR in mouse liver.Nucleic acids research · 2010Article
- Research Resource: The androgen receptor modulates expression of genes with critical roles in muscle development and function.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Emerging parallels between stomatal and muscle cell lineages.Plant physiology · 2009Article
- Comparative in silico analysis identifies bona fide MyoD binding sites within the Myocyte stress 1 gene promoter.BMC molecular biology · 2008Article
- MicroRNA regulation of cell lineages in mouse and human embryonic stem cells.Cell stem cell · 2008Article
- Nonviral gene transfer to skeletal, smooth, and cardiac muscle in living animals.American journal of physiology. Cell physiology · 2005Review
- Adult myogenesis in Drosophila melanogaster can proceed independently of myocyte enhancer factor-2.Genetics · 2005Article
- Functional improvement of mutant keratin cells on addition of desmin: an alternative approach to gene therapy for dominant diseases.Gene therapy · 2004Article
- Transcription enhancer factor 1 binds multiple muscle MEF2 and A/T-rich elements during fast-to-slow skeletal muscle fiber type transitions.Molecular and cellular biology · 2003Article
- Content and localization of myostatin in mouse skeletal muscles during aging, mechanical unloading and reloading.Journal of muscle research and cell motility · 2001Article
- Molecular cloning and characterization of OsPSK, a gene encoding a precursor for phytosulfokine-alpha, required for rice cell proliferation.Plant molecular biology · 2000Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The first 85 nt upstream of the transcription initiation site of the mouse desmin gene, which contain an E box (E1), the binding site of the helix-loop-helix myogenic regulators, are sufficient to confer low level muscle-specific expression. High levels of desmin expression are due to an enhancer, located between nucleotides -798 and -976, which contains an additional E box (E2) and a muscle-specific enhancer factor-2 (MEF-2) binding site. We have previously shown that both myoD and myogenin can bind to the proximal (E1) and distal (E2) boxes. Here we demonstrate that MEF-2C, a myocyte-restricted member of the MEF-2 family, can bind to the desmin MEF-2 site. Functional units for the enhancer activity required intact E2 and MEF-2 elements. The desmin enhancer can function relatively well with either the E2 box or the MEF-2 site and only mutation of both eliminates transcriptional enhancement; the presence of both of these elements is required for maximum enhancer activity. On the other hand, mutagenesis of just the proximal E1 box showed that this element is essential for desmin gene expression. Double mutations of E1 with E2 or MEF-2 sites suggested that, to achieve high levels of desmin gene expression, E1 serves most possibly as an intermediary for either E2 or MEF-2 enhancer elements to function. The location of the E1 site relative to the TATA box is crucial. Its activity is DNA turn- and distance-dependent. Furthermore, this box seems to be the main element for desmin transactivation by myoD and myogenin in 10T1/2 cells. Its inactivation diminishes the transactivation by these factors; MRF4 and Myf5, however, can still partially function, possibly by using the distal E2 box.
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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.