EC Number   |
Natural Substrates |
|---|
   3.4.22.54 | AHNAK nucleoprotein + H2O |
AHNAK is lost in cells expressing active CAPN3. Conversely, AHNAK accumulates when calpain 3 is defective in skeletal muscle of calpainopathy patients |
| 3.4.22.54 | alpha-actinin-3 + H2O |
- |
| 3.4.22.54 | alpha-fodrin + H2O |
- |
| 3.4.22.54 | beta-catenin + H2O |
calpain 3 specifically controls the level of membrane-associated beta-catenin and M-cadherin during myogenesis |
| 3.4.22.54 | connectin + H2O |
p94 binds to connectin at multiple sites including loci in the N2A and PEVK regions of connectin. Functionally, p94-N2A interactions suppress p94 autolysis and protected connectin from proteolysis. Dynamic nature of connectin molecule as a regulatory scaffold of p94 functions |
| 3.4.22.54 | cyclin A + H2O |
calpain 3-mediated cleavage of cyclin A in dividing myeloid pregenitor cells is important for the onset of differentiation |
| 3.4.22.54 | filamin C + H2O |
enzyme specifically cleaves the C-terminal portion in living cells. Filamin C may be an in vivo substrate to c3, functioning to regulate protein-protein interactions with the sarcoglycans |
| 3.4.22.54 | M-cadherin + H2O |
calpain 3 specifically controls the level of membrane-associated beta-catenin and M-cadherin during myogenesis |
| 3.4.22.54 | MARP2/Ankrd2 + H2O |
- |
| 3.4.22.54 | more |
a small in-frame deletion within the protease domain of muscle-specific calpain, p94 causes early-onset limb-girdle muscular dystrophy 2A |
