Activation of the AP-1 transcription factor by inflammatory cytokines of the TNF family

Gene Expr. 1999;7(4-6):217-31.


Inflammatory cytokines of the tumor necrosis factor (TNF) family mediate a large variety of cellular and organismal inflammatory responses and are important to the pathogenesis of a number of important disease states including arthritis, septic shock, inflammatory bowel disease, and, possibly, type II diabetes. Many of the responses to these cytokines require de novo gene expression mediated by the activator protein-1 (AP-1) heterodimeric transcription factor. This review will discuss what is known of how cytokines of the TNF family, acting at the cell surface, recruit two mitogen-activated protein kinase (MAPK) subfamilies, the stress-activated protein kinases (SAPKs, also called JNKs) and the p38s, to transduce signals to AP-1.

Publication types

  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Gene Expression Regulation
  • Humans
  • Mitogen-Activated Protein Kinases*
  • Molecular Sequence Data
  • Proteins / metabolism
  • Receptors, Tumor Necrosis Factor / metabolism
  • Signal Transduction*
  • TNF Receptor-Associated Factor 1
  • Transcription Factor AP-1 / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism*
  • p38 Mitogen-Activated Protein Kinases


  • Proteins
  • Receptors, Tumor Necrosis Factor
  • TNF Receptor-Associated Factor 1
  • Transcription Factor AP-1
  • Tumor Necrosis Factor-alpha
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases