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Logo of jcinvestThe Journal of Clinical Investigation
 
From:
Published online 2010 July 1. doi: 10.1172/JCI40658

Figure 2

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Exercise-induced myofiber degeneration in p94KI.

(A and B) Immunodetection of p94 and its fragments (black and white arrowheads, respectively) in WT, WT-ex, p94KI, and p94KI-ex mice. The Sup fraction from TA was subjected to Western blot analysis using an anti-pIS2C Ab (A). Hairlines indicate lanes that were run on the same gel but were noncontiguous. The p94 bands were quantified by normalizing to the CBB-stained actin (CBB in A) (B). cont, COS-expressed p94:C129S. *P < 0.01. (CN) Damaged myofibers in the gastrocnemius muscles from WT, WT-ex, p94KI, and p94KI-ex mice were detected by an anti-laminin α2 Ab (CF) and EBD autofluorescence (GJ). Merged images plus nuclei (KN). Scale bars: 100 μm. (O) Drastic increase in the serum CK level in p94KI-ex. Blood samples of WT-ex and p94KI-ex were taken immediately after excise. (P and Q) The proportion of CNM in p94KI was significantly increased after exercise. The TA (P) and soleus (Q) from WT, p94KI, WT-ex, and p94KI-ex sacrificed 10 days after exercise were analyzed. The proportion of CNMs was calculated as in Figure Figure1.1. *P < 0.05 versus WT; **P < 0.05 versus p94KI; ***P < 0.05 versus WT-ex.

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