Laboratory Animals > Volume 18, Number 1 > Pp. 1-6

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Watkins, W. J. Articles by Watts, D. C. Search for Related Content PubMed PubMed Citation Social Bookmarking                      What's this?

Biological features of the new A2G-adr mouse mutant with abnormal muscle function

W. Jean Watkins and D. C. Watts

Department of Biochemistry, Guy's Hospital Medical School, London SE1 9RT, UK; Department of Biochemistry, Guy's Hospital Medical School, London SE1 9RT, UK

A new mouse mutant (A2G-adr) with abnormal muscle function is described and has been compared with the 129 Re dystrophic mouse. The mutation, which is due to an autosomal gene defect, results in myotonic-like spasms, progressive muscle weakness and a reduced lifespan. Affected animals were consistently lighter than normal littermates; comparison of organ weights and organ-to-bodyweight ratios indicated a slower growth rate in the mutants.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				E. van Lunteren, J. Pollarine, and M. Moyer Isotonic contractile impairment due to genetic CLC-1 chloride channel deficiency in myotonic mouse diaphragm muscle Exp Physiol, July 1, 2007; 92(4): 717 - 729. [Abstract] [Full Text] [PDF]