Key result
Dystrophic mouse skeletal muscle shows severalfold higher ribonuclease II activity and lacks normal inhibitor unlike heart.
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Muscle-specific RNase dysregulation in dystrophic mice is hypothesis-generating; leaves open its role in human muscular dystrophy.
Skeletal muscle extracts from mice with muscular dystrophy contain severalfold higher than normal levels of free alkaline ribonuclease II activity and none of the free ribonuclease inhibitor normally present. This abnormal pattern is not seen in heart or liver extracts from dystrophic mice.
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Little et al. (1970) studied this question. Dystrophic mouse skeletal muscle contains severalfold higher levels of free alkaline ribonuclease II activity and lacks normal free ribonuclease inhibitor, unlike heart or liver.
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