Signaling from toxic metals to NF-κB and beyond: Not just a matter of reactive oxygen species

Fei Chen, Xianglin Shi

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

The nuclear factor kappa B (NF-κB) family of transcription factors controls expression of a number of early response genes associated with inflammatory responses, cell growth, cell cycle progression, and neoplastic transformation. These genes include a multitude of cytokines, chemokines, adhesion molecules, immune receptors, stress proteins, apoptotic or anti-apoptotic regulators, and several oncogenes. Accumulating evidence indicates that a variety of toxic metals are able to affect the activation or activity of NF-κB, but the molecular mechanisms involved in this process remain largely unknown. The signaling pathways mediating cytokine- or microorganism-induced NF-κB activation have been well established recently. Whether the same signaling systems are involved in metal-induced NF-κB activation, however, is unclear. In the present review, we have attempted to evaluate and update the possible mechanisms of signals on the activation and function of NF-κB.

Original languageEnglish
Pages (from-to)807-811
Number of pages5
JournalEnvironmental Health Perspectives
Volume110
Issue numberSUPPL. 5
DOIs
StatePublished - Oct 2002

Keywords

  • Kinase
  • Metals
  • NF-κB
  • Oxidative stress
  • Signal transduction

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

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