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Fig. 5. Knock-down of MURF-2 levels specifically disrupts M-line region components of myofibrils, but not Z-lines or thick filament components. Chick cardiac myocytes were treated with antisense oligonucleotides to MURF-2 or control oligonucleotides, fixed 48 hours later, and stained for various sarcomeric components. Control myocytes exhibited bright staining for MURF-2 and staining for 
-actinin, the peripheral Z-line region of titin (T11 epitope), myosin, and the M-line components myomesin and the M-line region of titin (AB5) in regular, striated patterns (a-c, g-i). Myocytes that had knocked-down levels of MURF-2 (d) exhibited staining for -actinin, titin T11, and myosin in regular, striated patterns (e,f,j). However, in 
80% of the antisense-treated myocytes, staining for the M-line components myomesin and the C-terminal region of titin was strikingly disrupted (k,l). Double arrows point to regular striations and single arrowheads point to disrupted myofibrils. (B) Human GFP-MURF-2 expression rescues myomesin staining in antisense-treated chick myocytes. Chick cardiac myocytes co-transfected with MURF-2 antisense oligos and human GFP-MURF-2 were co-stained for myomesin. Myocytes expressing GFP-hMURF-2 (m) contained regular, striated myomesin staining (n), compared to antisense-treated myocytes not expressing GFP-h-MURF-2 (k). Bar, 10 µm.
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