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

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 hum...

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Veröffentlicht in:	Human molecular genetics 2003-10, Vol.12 (19), p.2467-2479
Hauptverfasser:	Moghadaszadeh, Behzad, Albrechtsen, Reidar, Guo, Ling T, Zaik, Michaela, Kawaguchi, Nobuko, Borup, Rehannah H, Kronqvist, Pauliina, Schroder, Henrik D, Davies, Kay E, Voit, Thomas, Nielsen, Finn C, Engvall, Eva, Wewer, Ulla M
Format:	Artikel
Sprache:	eng
Schlagworte:	ADAM Proteins ADAM12 Protein Animals Biomarkers Cytoskeletal Proteins - biosynthesis Dystrophin - deficiency Gene Expression Profiling Glycoproteins - biosynthesis Immunoblotting Immunohistochemistry Integrin alpha Chains - biosynthesis Membrane Proteins - biosynthesis Membrane Proteins - metabolism Metalloendopeptidases - metabolism Mice Mice, Inbred mdx Mice, Transgenic Muscle, Skeletal - metabolism Oligonucleotide Array Sequence Analysis Precipitin Tests Tissue Distribution Transgenes Up-Regulation Utrophin
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