Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1016/s0014-5793(03)00175-3

Type

Journal article

Journal

FEBS Lett

Publication Date

13/03/2003

Volume

538

Pages

168 - 172

Keywords

Animals, Base Sequence, Cell Line, Cytoskeletal Proteins, Electrophoretic Mobility Shift Assay, Endothelium, Gene Expression Regulation, Humans, Membrane Proteins, Mice, Molecular Sequence Data, Promoter Regions, Genetic, Sequence Homology, Nucleic Acid, Tetradecanoylphorbol Acetate, Transcription Factors, Transcriptional Activation, Utrophin