ArticleNucleic acids research2001
The role of basal and myogenic factors in the transcriptional activation of utrophin promoter A: implications for therapeutic up-regulation in Duchenne muscular dystrophy.
Article in Nucleic acids research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 40 citations in OpenAlex.
- CRISPR-Cas9-mediated upregulation of utrophin ameliorates Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Myotendinous Junction development and repair.Journal of orthopaedic translation · 2026Review
- Endogenous bioluminescent reporters reveal a sustained increase in utrophin gene expression upon EZH2 and ERK1/2 inhibition.Communications biology · 2023Article
- Targeting IRES-dependent translation as a novel approach for treating Duchenne muscular dystrophy.RNA biology · 2021Review
- Identification of therapeutics that target eEF1A2 and upregulate utrophin A translation in dystrophic muscles.Nature communications · 2020Article
- Alternative utrophin mRNAs contribute to phenotypic differences between dystrophin-deficient mice and Duchenne muscular dystrophy.FEBS letters · 2018Article
- Article
- Combinatorial therapeutic activation with heparin and AICAR stimulates additive effects on utrophin A expression in dystrophic muscles.Human molecular genetics · 2016Article
- Cis-Acting Sequence Elements and Upstream Open Reading Frame in Mouse Utrophin-A 5'-UTR Repress Cap-Dependent Translation.PloS one · 2015Article
- Detection of interacting transcription factors in human tissues using predicted DNA binding affinity.BMC genomics · 2012Article
- Translational regulation of utrophin by miRNAs.PloS one · 2011Article
- Targeting artificial transcription factors to the utrophin A promoter: effects on dystrophic pathology and muscle function.The Journal of biological chemistry · 2008Article
- Modulation of utrophin A mRNA stability in fast versus slow muscles via an AU-rich element and calcineurin signaling.Nucleic acids research · 2008Article
- Ets-2 repressor factor silences extrasynaptic utrophin by N-box mediated repression in skeletal muscle.Molecular biology of the cell · 2007Article
- The GTPase RhoA increases utrophin expression and stability, as well as its localization at the plasma membrane.The Biochemical journal · 2005Article
- Therapeutics for Duchenne muscular dystrophy: current approaches and future directions.Journal of molecular medicine (Berlin, Germany) · 2004Review
- Expression of utrophin A mRNA correlates with the oxidative capacity of skeletal muscle fiber types and is regulated by calcineurin/NFAT signaling.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked recessive muscle wasting disease caused by the absence of a muscle cytoskeletal protein, dystrophin. Utrophin is the autosomal homologue of dystrophin. We previously demonstrated that overexpression of utrophin in the muscles of dystrophin-null transgenic mice completely prevented the phenotype arising from dystrophin deficiency. Two independently regulated promoters control utrophin expression and the upstream promoter (promoter A) is synaptically regulated in muscle. In this study, we have investigated basal regulation and myogenic induction of promoter A. Interactions between Ap2 and Sp1 and their cognate DNA motifs are critical for basal transcription from the minimal promoter region. During differentiation of C2C12 myoblasts in vitro, a 2-fold increase in A-utrophin mRNA level was observed. Expression of a reporter gene, whose transcription was driven by a 1.3 kb promoter A fragment, paralleled expression of the endogenous transcript. Myogenic induction mapped to a conserved upstream muscle-specific E-box, which was shown to bind myogenic regulatory factors, transactivating the promoter up to 18-fold in transient assays. This study provides a basis for further understanding the regulatory mechanisms that control utrophin expression in muscle and may facilitate the development of reagents to effect therapeutic up-regulation of utrophin in DMD.
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