Regulation of STAT-dependent pathways by growth factors and cytokines

FASEB J. 1996 Dec;10(14):1578-88.

Abstract

Polypeptide growth factors and cytokines elicit their effects by activating specific cell-surface receptors, thereby initiating signaling cascades that culminate in the induction of specific subsets of genes. Initially identified as the primary mediators of interferon-dependent signaling, JAKs and STATs are now known to be utilized by many different extracellular signaling proteins. In this report we describe how JAK-STAT pathways transduce signals initiated by both cytokines and growth factors, focusing on how specificity is achieved through STAT-receptor interactions and on how receptor-associated kinases function in STAT activation. We also summarize current information on interactions between signaling pathways, particularly STAT-Ras cross-talk and the relative importance of these two pathways in regulating the transcription of target genes.

Publication types

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

MeSH terms

  • Animals
  • Cytokines / metabolism*
  • DNA-Binding Proteins / metabolism*
  • Growth Substances / metabolism*
  • Humans
  • Interferons / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Receptors, Cytokine / metabolism
  • STAT1 Transcription Factor
  • Signal Transduction / physiology*
  • Trans-Activators / metabolism*
  • Transcription, Genetic

Substances

  • Cytokines
  • DNA-Binding Proteins
  • Growth Substances
  • Receptors, Cytokine
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • Trans-Activators
  • Interferons
  • Protein-Tyrosine Kinases
  • Receptor Protein-Tyrosine Kinases