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Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
Published on: March 16, 2017
Protein S-nitrosylation: a physiological signal for neuronal nitric oxide
S R Jaffrey1, H Erdjument-Bromage, C D Ferris
1Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Nitric oxide (NO) is involved in many body processes. This study reveals that NO modifies proteins via S-nitrosylation, a key signaling pathway for neuronal NO synthase (nNOS).
Area of Science:
- Biochemistry
- Molecular Biology
- Physiology
Background:
- Nitric oxide (NO) has established roles in physiology and pathophysiology, primarily through soluble guanylyl cyclase activation.
- The role of endogenous NO in protein S-nitrosylation, a post-translational modification, remains unclear.
- Neuronal nitric oxide synthase (nNOS) is a key source of endogenous NO in the nervous system.
Purpose of the Study:
- To investigate the physiological relevance of endogenous protein S-nitrosylation.
- To identify endogenous S-nitrosylated proteins and their functions.
- To determine the role of neuronal NO synthase (nNOS) in protein S-nitrosylation.
Main Methods:
- Development of a novel proteomic approach to identify S-nitrosylated proteins.
- Analysis of protein S-nitrosylation in wild-type and nNOS-deficient mice.
- Characterization of identified S-nitrosylated proteins.
Main Results:
- Identification of a significant population of endogenously S-nitrosylated proteins.
- Demonstration of reduced S-nitrosylation in mice lacking nNOS, confirming nNOS as a source.
- Inclusion of metabolic, structural, and signaling proteins among NO targets.
- These proteins may act as effectors for neuronally derived NO.
Conclusions:
- Protein S-nitrosylation is a significant physiological signaling mechanism mediated by nNOS.
- Endogenous NO, via nNOS, directly modifies proteins, expanding its known biological functions.
- This discovery opens new avenues for understanding NO-mediated cellular regulation and disease.
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