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Protein S-nitrosylation: purview and parameters
TLDR
S-nitrosylation conveys a large part of the ubiquitous influence of nitric oxide on cellular signal transduction, and provides a mechanism for redox-based physiological regulation. Expand
A metabolic enzyme for S-nitrosothiol conserved from bacteria to humans
TLDR
It is concluded that GSNO reductase is evolutionarily conserved from bacteria to humans, is critical for SNO homeostasis, and protects against nitrosative stress. Expand
Biochemistry of nitric oxide and its redox-activated forms.
TLDR
The integration of this chemistry with current perspectives of NO biology illuminates many aspects of NO biochemistry, including the enzymatic mechanism of synthesis, the mode of transport and targeting in biological systems, the means by which its toxicity is mitigated, and the function-regulating interaction with target proteins. Expand
Nitrosylation The Prototypic Redox-Based Signaling Mechanism
TLDR
Whereas phosphorylation clearly Spain lies at the heart of many signal transduction pathways, has been expanded re-translational modification of proteins, are conserved cently by the discovery of an enzymatic function for throughout evolution and influence most aspects of cel-hemoglobin. Expand
Nitric oxide in skeletal muscle
TLDR
It is shown that rat skeletal muscle expresses neuronal-type NO synthase and that activity varies among several respiratory and limb muscles, and that two physiological functions of NO in skeletal muscle are supported. Expand
Physiology of nitric oxide in skeletal muscle.
TLDR
These studies provide new insights into fundamental aspects of muscle physiology, cell biology, ion channel physiology, calcium homeostasis, signal transduction, and the biochemistry of redox-related systems. Expand
Activation of the cardiac calcium release channel (ryanodine receptor) by poly-S-nitrosylation.
TLDR
Results reveal that ion channels can differentiate nitrosative from oxidative signals and indicate that the cardiac calcium release channel (ryanodine receptor) in canines is regulated by posttranslational chemical modification(s) of sulfurs. Expand
Identification of the enzymatic mechanism of nitroglycerin bioactivation
TLDR
These results demonstrate that the biotransformation of GTN occurs predominantly in mitochondria through a novel reductase action of mtALDH and suggest that nitrite is an obligate intermediate in generation of NO bioactivity. Expand
A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds
TLDR
It is reported that NO.-mediated neurotoxicity is engendered, at least in part, by reaction with superoxide anion (O.-2), apparently leading to formation of peroxynitrite (ONOO−), and not by NO. Expand
S-nitrosylation of proteins with nitric oxide: synthesis and characterization of biologically active compounds.
TLDR
It is demonstrated that S-nitroso proteins form readily under physiologic conditions and possess EDRF-like effects of vasodilation and platelet inhibition, suggesting that S -nitrosothiol groups in proteins may serve as intermediates in the cellular metabolism of NO and raise the possibility of an additional type of cellular regulatory mechanism. Expand
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