From receptors to stress-activated MAP kinases

Oncogene. 1999 Nov 1;18(45):6087-93. doi: 10.1038/sj.onc.1203129.

Abstract

The cell signaling pathways that culminate in activation of a family of stress-activated MAP kinases are beginning to be defined. Determination of cell life and cell death is known to largely depend on the balance of intrinsic life and death signals within cells. Recently, two representative mammalian stress-activated kinases, the JNK and p38 MAP kinases, have been implicated in determination of cell fate by modifying the life, death and differentiation signals. However, the molecular mechanisms by which extracellular signals are transmitted from membrane receptors to the most upstream kinases in the JNK and p38 signaling modules are not fully understood. This review will provide an overview of current knowledge of molecular links between inflammatory cytokine receptors and stress-activated MAP kinase cascades.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Carrier Proteins / metabolism
  • GTP-Binding Proteins / metabolism
  • Interleukin-1 / pharmacology
  • JNK Mitogen-Activated Protein Kinases*
  • MAP Kinase Kinase 4
  • MAP Kinase Kinase Kinases / metabolism
  • MAP Kinase Signaling System* / drug effects
  • Mitogen-Activated Protein Kinase Kinases / metabolism*
  • Mitogen-Activated Protein Kinases / metabolism*
  • Receptors, Tumor Necrosis Factor / metabolism
  • Thioredoxins / metabolism
  • fas Receptor / metabolism
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Carrier Proteins
  • Interleukin-1
  • Receptors, Tumor Necrosis Factor
  • fas Receptor
  • Thioredoxins
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase Kinases
  • MAP Kinase Kinase 4
  • Mitogen-Activated Protein Kinase Kinases
  • GTP-Binding Proteins