Key result
Nitric oxide donors inhibited the cleavage of dystrophin by coxsackievirus B protease 2A in a dose-dependent manner (IC50, 51 micromol/L) through S-nitrosylation of the active-site cysteine.
Why the study?
Does nitric oxide inhibit dystrophin proteolysis by coxsackieviral protease 2A in vitro and in cell models?
Does nitric oxide inhibit dystrophin proteolysis by coxsackieviral protease 2A in vitro and in cell models?
Effect estimate: IC50 51 micromol/L
Nitric oxide inactivates coxsackieviral protease 2A via S-nitrosylation, preventing dystrophin cleavage, which may offer a protective mechanism in enterovirus-induced cardiomyopathy.
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May protect against dystrophin cleavage in enteroviral models; hypothesis-generating, requires in vivo and clinical validation before any therapeutic consideration.
Badorff et al. (2000) studied Enterovirus-induced cardiomyopathy. Nitric oxide (NO) donors was evaluated on Cleavage of dystrophin by recombinant coxsackievirus B protease 2A (IC50 51 micromol/L). Nitric oxide donors inhibited the cleavage of dystrophin by coxsackievirus B protease 2A in a dose-dependent manner (IC50, 51 micromol/L) through S-nitrosylation of the active-site cysteine.
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