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Fig. 1. Upregulation of integrin {alpha}7 where sarcoglycan level is reduced. Immunoblotting of microsomal membrane fractions purified from skeletal muscle from mice lacking sarcoglycan subunits or dystrophin. The antibodies used are specific to the integrin {alpha}7 splice forms (Itg{alpha}7A and Itg{alpha}7B) representing splice variants that alter the cytoplasmic domains of integrin {alpha}7 (Mayer et al., 1997). A Coomassie blue-stained loading control is shown in the lower panel of each blot. (A) Upregulation of integrin {alpha}7 in muscle null for {delta}-sarcoglycan (dsg–/–). (B) Upregulation of integrin {alpha}7 in muscle null for {gamma}-sarcoglycan (gsg–/–) and in dystrophin-null mdx muscle. mdx mice have a secondary reduction of sarcoglycan at the plasma membrane (Ohlendieck and Campbell, 1991). (C) Graphical representation of integrin {alpha}7 expression from blots shown in A and B. Upregulation of integrin {alpha}7 was seen in all three mutant models but was greatest in muscle lacking {delta}-sarcoglycan (dsg–/–) where sarcoglycan loss is greatest (Hack et al., 2000b).