Key result
In mouse myotubes, nitric oxide synthase activity mediates calcium-induced phosphorylation of GSK-3beta and activation of NFAT-dependent transcription in a guanylate cyclase-dependent manner.
Population
C2C12 myotubes (mouse skeletal muscle cells)
Comparison
Calcium ionophore A23187 or thapsigargin, NO… vs Untreated cells or cells treated with calcium…
Design
Preclinical
Authors
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No immediate clinical implications; leaves open whether this NO-GSK-3β-NFAT pathway modulates human muscle adaptation or disease.
Nitric oxide mediates calcium-induced phosphorylation of GSK-3beta and activation of NFAT-dependent transcription in skeletal muscle myotubes via a guanylate cyclase-dependent mechanism.
Drenning et al. (2008) studied this question. Nitric oxide and calcium ionophores was evaluated on NFAT transcriptional activity and GSK-3beta phosphorylation. In mouse myotubes, nitric oxide synthase activity mediates calcium-induced phosphorylation of GSK-3beta and activation of NFAT-dependent transcription in a guanylate cyclase-dependent manner.
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