Key result
The S1412D mutation in nNOS speeds electron transfer and intrinsic NO synthesis but diminishes NO release in the steady state, revealing the importance of heme reduction rate.
Population
Rat neuronal NO synthase (nNOS)
Comparison
Ser-1412 to Asp mutation in the reductase domain vs Wild-type nNOS
Design
Preclinical
Authors
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No immediate clinical relevance; extends mechanistic understanding of nNOS heme reduction in animal models.
The S1412D mutation in nNOS demonstrates that the rate of heme reduction is critical in controlling steady-state NO synthesis and release.
Adak et al. (2001) studied this question. S1412D mutation in rat neuronal NO synthase (nNOS) vs. Wild-type nNOS was evaluated on Catalytic parameters including heme reduction, NO complex formation, and steady-state NO synthesis. The S1412D mutation in nNOS speeds electron transfer and intrinsic NO synthesis but diminishes NO release in the steady state, revealing the importance of heme reduction rate.
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