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Compensation for dystrophin-deficiency: ADAM12 overexpression in skeletal muscle results in increased alpha 7 integrin, utrophin and associated glycoproteins.

Abstract:

Mouse models for genetic diseases are among the most powerful tools available for developing and testing new treatment strategies. ADAM12 is a disintegrin and metalloprotease, previously demonstrated to significantly alleviate the pathology of mdx mice, a model for Duchenne muscular dystrophy in humans. More specifically ADAM12 appeared to prevent muscle cell necrosis in the mdx mice as evidenced by morphological analysis and by the reduced levels of serum creatine kinase. In the present stud...

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Publication status:
Published

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Publisher copy:
10.1093/hmg/ddg264

Authors


Moghadaszadeh, B More by this author
Albrechtsen, R More by this author
Kawaguchi, N More by this author
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Journal:
Human molecular genetics
Volume:
12
Issue:
19
Pages:
2467-2479
Publication date:
2003-10-05
DOI:
EISSN:
1460-2083
ISSN:
0964-6906
URN:
uuid:19d87fd3-c7d3-420c-97c5-f384b8ac7d7a
Source identifiers:
106667
Local pid:
pubs:106667

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