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Protein Transnitrosylation Signaling Networks Contribute to Inflammaging and Neurodegenerative Disorders.

Tomohiro Nakamura1, Chang-Ki Oh1, Xu Zhang1

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Antioxidants & Redox Signaling
|May 7, 2021
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Nitric oxide (NO) signaling, crucial in the nervous system, is altered in aging and neurodegenerative diseases. Protein S-nitrosylation, particularly via transnitrosylation, emerges as a key mechanism in neurodegeneration and synaptic damage.

Keywords:
S-nitrosylationneurodegenerative diseasesnitric oxidetransnitrosylation

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Area of Science:

  • Biochemistry
  • Neuroscience
  • Redox Biology

Background:

  • Physiological nitric oxide (NO) and reactive nitrogen species (RNS) regulate neural signaling.
  • Dysregulated RNS contribute to neuronal loss in aging (inflammaging) and neurodegenerative diseases.
  • Protein S-nitrosylation (SNO) is a primary NO signaling mechanism, often occurring via transnitrosylation.

Purpose of the Study:

  • To review the chemical biology of protein transnitrosylation.
  • To highlight its role in mediating redox-dependent signaling in health and disease.
  • To discuss its implications in aging, inflammation, and neurodegeneration.

Main Methods:

  • Review of existing literature on S-nitrosylation and transnitrosylation.
  • Analysis of identified transnitrosylation networks (e.g., Uch-L1-Cdk5-Drp1).
  • Discussion of the chemical mechanisms of transnitrosylation.

Main Results:

  • Transnitrosylation is a critical mechanism for transferring redox signals between proteins.
  • A novel tricomponent transnitrosylation network (Uch-L1-Cdk5-Drp1) mediates synaptic damage in Alzheimer's disease.
  • Protein transnitrosylation links aging, inflammation, and neurodegeneration.

Conclusions:

  • Protein transnitrosylation is a key pathway in neurodegenerative processes.
  • Understanding transnitrosylation is crucial for developing therapeutic strategies.
  • Further research into protein transnitrosylation is needed to elucidate its role in neuronal function and disease.