Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

G-Utrophin, the autosomal homologue of dystrophin Dp116, is expressed in sensory ganglia and brain

Blake, Derek J., Schofield, Julian N., Zuellig, Richard A., Górecki, Dariusz C., Phelps, S. R., Barnard, E. A., Edwards, Y. H. and Davies, Kay E. 1995. G-Utrophin, the autosomal homologue of dystrophin Dp116, is expressed in sensory ganglia and brain. Proceedings of the National Academy of Sciences of the United States of America 92 (9) , pp. 3697-3701. 10.1073/pnas.92.9.3697

Full text not available from this repository.


The utrophin gene is closely related to the dystrophin gene in both sequence and genomic structure. The Duchenne muscular dystrophy (DMD) locus encodes three 14-kb dystrophin transcripts in addition to several smaller isoforms, one of which, Dp116, is specific to peripheral nerve. We describe here the corresponding 5.5-kb mRNA from the utrophin locus. This transcript, designated G-utrophin, is of particular interest because it is specifically expressed in the adult mouse brain and appears to be the predominant utrophin transcript in this tissue. G-utrophin is expressed in brain sites generally different from the regions expressing beta-dystroglycan. During mouse embryogenesis G-utrophin is also seen in the developing sensory ganglia. Our data confirm the close evolutionary relationships between the DMD and utrophin loci; however, the functions for the corresponding proteins probably differ.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Subjects: R Medicine > R Medicine (General)
Uncontrolled Keywords: Duchenne muscular dystrophy, alternative transcript, mouse development, neuron
Publisher: National Academy of Sciences
ISSN: 0027-8424
Last Modified: 04 Jun 2017 05:12

Citation Data

Cited 64 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item