Abstract
Duchenne muscular dystrophy is caused by dystrophin deficiency, which can be prevented in the mdx mouse model by over-expression of an autosomal homologue, utrophin. Utrophin has two characterised full-length promoters, A and B. No data are available on the transcriptional regulation of B utrophin, which has been recently localised to the endothelium. Similar to characterised endothelial promoters, Ets and Ap-1 individually trans-activate the human B core promoter. Synergistic activation by GATA-2 and c-jun to the order of 20-fold was observed.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Cell Line
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Cytoskeletal Proteins / genetics*
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Electrophoretic Mobility Shift Assay
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Endothelium / metabolism
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Gene Expression Regulation / drug effects*
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Humans
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Membrane Proteins / genetics*
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Mice
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Molecular Sequence Data
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Promoter Regions, Genetic
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Sequence Homology, Nucleic Acid
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Tetradecanoylphorbol Acetate / pharmacology
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Transcription Factors / physiology*
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Transcriptional Activation / drug effects
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Utrophin
Substances
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Cytoskeletal Proteins
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Membrane Proteins
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Transcription Factors
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Utrn protein, mouse
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Utrophin
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Tetradecanoylphorbol Acetate