SOD1 wt or SOD1G93A transgenic mouse, transfected with human wt SOD1 or human SOD1G93A
flexor digitorum brevis (FDB) muscles
Zhou J et al.(2010) Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis J. Biol. Chem. 285: 705-712
Greater increase in cytosolic Ca2(+), likely caused by greater Ca2+ release in response to stimuli in regions with depolarized mitochondria, appears to be a characteristic feature of the affected muscle in the ALS mouse model. This Ca2(+) regulatory defect is likely to result from mitochondrial defects.
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