Signal Transduction by the c-Jun N-terminal Kinase (JNK)--from Inflammation to Development

Curr Opin Cell Biol. 1998 Apr;10(2):205-19. doi: 10.1016/s0955-0674(98)80143-9.

Abstract

The c-Jun amino-terminal kinase (JNK) group of MAP kinases has been identified in mammals and insects. JNK is activated by exposure of cells to cytokines or environmental stress, indicating that this signaling pathway may contribute to inflammatory responses. Genetic and biochemical studies demonstrate that this signaling pathway also regulates cellular proliferation, apoptosis, and tissue morphogenesis. A functional role for JNK is therefore established in both the cellular response to stress and in many normal physiological processes.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases / physiology*
  • Embryo, Mammalian / enzymology
  • Embryo, Mammalian / physiology
  • Embryo, Nonmammalian / enzymology
  • Embryo, Nonmammalian / physiology
  • Humans
  • Inflammation / enzymology*
  • Inflammation / metabolism
  • Inflammation / physiopathology
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases*
  • Morphogenesis / physiology*
  • Signal Transduction / physiology*

Substances

  • Calcium-Calmodulin-Dependent Protein Kinases
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases