ArticleProceedings of the National Academy of Sciences of the United States of America1999
A second promoter provides an alternative target for therapeutic up-regulation of utrophin in Duchenne muscular dystrophy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 102 citations in OpenAlex.
- Enhanced recovery of terminal sequences of viral RNAs via fine-tuning of the high-throughput sequencing library preparation and evidence of a non-templated nucleotide addition at the 3' end of the minus strand in members of the genusThe Journal of general virology · 2026Article
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- Endogenous bioluminescent reporters reveal a sustained increase in utrophin gene expression upon EZH2 and ERK1/2 inhibition.Communications biology · 2023Article
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 2023Review
- Identifying FDA-Approved Drugs that Upregulate Utrophin A as a Therapeutic Strategy for Duchenne Muscular Dystrophy.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Utrophin modulator drugs as potential therapies for Duchenne and Becker muscular dystrophies.Neuropathology and applied neurobiology · 2021Article
- Targeting IRES-dependent translation as a novel approach for treating Duchenne muscular dystrophy.RNA biology · 2021Review
- PMO-based let-7c site blocking oligonucleotide (SBO) mediated utrophin upregulation in mdx mice, a therapeutic approach for Duchenne muscular dystrophy (DMD).Scientific reports · 2020Article
- Genome Editing-Mediated Utrophin Upregulation in Duchenne Muscular Dystrophy Stem Cells.Molecular therapy. Nucleic acids · 2020Article
- Identification of therapeutics that target eEF1A2 and upregulate utrophin A translation in dystrophic muscles.Nature communications · 2020Article
- High-throughput identification of post-transcriptional utrophin up-regulators for Duchenne muscle dystrophy (DMD) therapy.Scientific reports · 2020Article
- Alternative utrophin mRNAs contribute to phenotypic differences between dystrophin-deficient mice and Duchenne muscular dystrophy.FEBS letters · 2018Article
- Article
- Spell Checking Nature: Versatility of CRISPR/Cas9 for Developing Treatments for Inherited Disorders.American journal of human genetics · 2016Article
- Cis-Acting Sequence Elements and Upstream Open Reading Frame in Mouse Utrophin-A 5'-UTR Repress Cap-Dependent Translation.PloS one · 2015Article
- Identification of a secondary promoter of CASP8 and its related transcription factor PURα.International journal of oncology · 2014Article
- Genome-wide genetic associations with IFNγ response to smallpox vaccine.Human genetics · 2012Article
- Drug discovery for Duchenne muscular dystrophy via utrophin promoter activation screening.PloS one · 2011Article
- Translational regulation of utrophin by miRNAs.PloS one · 2011Article
- Dynamic functional modules in co-expressed protein interaction networks of dilated cardiomyopathy.BMC systems biology · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is an inherited muscle-wasting disease caused by the absence of a muscle cytoskeletal protein, dystrophin. We have previously shown that utrophin, the autosomal homologue of dystrophin, is able to compensate for the absence of dystrophin in a mouse model of DMD; we have therefore undertaken a detailed study of the transcriptional regulation of utrophin to identify means of effecting its up-regulation in DMD muscle. We have previously isolated a promoter element lying within the CpG island at the 5' end of the gene and have shown it to be synaptically regulated in vivo. In this paper, we show that there is an alternative promoter lying within the large second intron of the utrophin gene, 50 kb 3' to exon 2. The promoter is highly regulated and drives transcription of a widely expressed unique first exon that splices into a common full-length mRNA at exon 3. The two utrophin promoters are independently regulated, and we predict that they respond to discrete sets of cellular signals. These findings significantly contribute to understanding the molecular physiology of utrophin expression and are important because the promoter reported here provides an alternative target for transcriptional activation of utrophin in DMD muscle. This promoter does not contain synaptic regulatory elements and might, therefore, be a more suitable target for pharmacological manipulation than the previously described promoter.
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