Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2002 Nov;14(11):879-97.
doi: 10.1016/s0898-6568(02)00053-0.

Antioxidant and prooxidant mechanisms in the regulation of redox(y)-sensitive transcription factors

Affiliations
Review

Antioxidant and prooxidant mechanisms in the regulation of redox(y)-sensitive transcription factors

John J Haddad. Cell Signal. 2002 Nov.

Abstract

A progressive rise of oxidative stress due to the altered reduction-oxidation (redox) homeostasis appears to be one of the hallmarks of the processes that regulate gene transcription in physiology and pathophysiology. Reactive oxygen (ROS) and nitrogen (RNS) species serve as signaling messengers for the evolution and perpetuation of the inflammatory process that is often associated with the condition of oxidative stress, which involves genetic regulation. Changes in the pattern of gene expression through ROS/RNS-sensitive regulatory transcription factors are crucial components of the machinery that determines cellular responses to oxidative/redox conditions. Transcription factors that are directly influenced by reactive species and pro-inflammatory signals include nuclear factor-kappaB (NF-kappaB) and hypoxia-inducible factor-1alpha (HIF-1alpha). Here, I describe the basic components of the intracellular oxidative/redox control machinery and its crucial regulation of oxygen- and redox-sensitive transcription factors such as NF-kappaB and HIF-1alpha.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources