General Information:

Id: 1,459 (click here to show other Interactions for entry)
Diseases: Amyotrophic lateral sclerosis
Mus musculus
SOD1 wt or SOD1G93A transgenic mouse, transfected with human wt SOD1 or human SOD1G93A
flexor digitorum brevis (FDB) muscles
article
Reference: 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 [PMID: 19889637]

Interaction Information:

Comment 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.
Formal Description
Interaction-ID: 10309

gene/protein mutant

SOD1-p.G93A

increases_quantity of

drug/chemical compound

Ca2+

in cytosol