Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Apr 13;21(8):2703. doi: 10.3390/ijms21082703

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2020 by the author.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Redox-control in the NO Pathway. Redox-dependent pathways that regulate nitric oxide (NO) and vascular homeostasis. The endothelial nitric oxide synthase (eNOS) and the soluble guanylyl cyclase (sGC) present a number of redox switches, which act directly or indirectly (for instance, in the case of the 26S proteasome, which is activated via 3-nitrotyrosine (3NT) modification causing inactivation of the eNOS cofactor tetrahydrobiopterin (BH₄) synthase GTP-cyclohydrolase (GCH-1), and of BH4 recycling enzyme dihydrofolate reductase (DHFR). Oxidation of BH₄ causes a positive feedback mechanism leading to further oxidative stress. Red arrows indicate inhibition. In contrast, NO prevents proteasomal DHFR degradation via tyrosine nitration of the 26S proteasome. O2⁻: superoxide anion; -SNO: s-nitroso-thiols; -SOxH: oxidized thiol; -SSG: glutathione disulfide; ZnC: Zinc; pThyr: phosphorylated thyrosine.