[HTML][HTML] Guanylyl cyclase sensitivity to nitric oxide is protected by a thiol oxidation-driven interaction with thioredoxin-1
Nitric oxide (NO) modulates many physiological events through production of cGMP from its
receptor, the NO-sensitive guanylyl cyclase (GC1). NO also appears to function in a cGMP-
independent manner, via S-nitrosation (SNO), a redox-based modification of cysteine thiols.
Previously, we have shown that S-nitrosated GC1 (SNO-GC1) is desensitized to NO
stimulation following prolonged NO exposure or under oxidative/nitrosative stress. In animal
models of nitrate tolerance and angiotensin II-induced hypertension, decreased vasodilation …
receptor, the NO-sensitive guanylyl cyclase (GC1). NO also appears to function in a cGMP-
independent manner, via S-nitrosation (SNO), a redox-based modification of cysteine thiols.
Previously, we have shown that S-nitrosated GC1 (SNO-GC1) is desensitized to NO
stimulation following prolonged NO exposure or under oxidative/nitrosative stress. In animal
models of nitrate tolerance and angiotensin II-induced hypertension, decreased vasodilation …