The role of NF-κB in the regulation of cell stress responses

Tieli Wang, Xia Zhang, Jian-Jian Li

Research output: Contribution to journalArticle

254 Scopus citations

Abstract

Nuclear factor-κB (NF-κB) is one of the key regulatory molecules in oxidative stress-induced cell activation. NF-κB is normally sequestered in the cytoplasm of nonstimulated cells and must translocate into the nucleus to regulate effector gene expression. A family of inhibitory proteins, IκBs, binds to NF-κB and masks its nuclear localization signal domain and therefore controls the translocation of NF-κB. Exposure of cells to extracellular stimuli that perturb redox balance results in rapid phosphorylation, ubiquitination, and proteolytic degradation of IκBs. This process frees NF-κB from the NF-κB/IκB complexes and enables NF-κB to translocate to the nucleus where it regulates gene transcription. Many effector genes including those encoding cytokines and adhesion molecules are in turn regulated by NF-κB. NF-κB is also an essential component of ionizing radiation (IR)-triggered signal transduction pathways that can lead to cell death or survival. The purpose of this review is to briefly summarize the recent progress in the studies of the role of reactive oxygen species (ROS), cytokines and ionizing radiation in NF-κB activation.

Original languageEnglish (US)
Pages (from-to)1509-1520
Number of pages12
JournalInternational Immunopharmacology
Volume2
Issue number11
DOIs
StatePublished - Oct 2002
Externally publishedYes

Keywords

  • Antioxidant responses
  • NF-κB
  • Oxidative stress
  • Signal transduction
  • Transcription factors

ASJC Scopus subject areas

  • Immunology
  • Pharmacology

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