Aberrant activation of JAK/STAT pathway components in response to G-CSF, interferon-alpha/beta and interferon-gamma in NFS-60 cells

Growth Factors. 1996;13(3-4):251-60. doi: 10.3109/08977199609003226.

Abstract

There is evidence that the cellular responses to cytokines, such as granulocyte colony stimulating factor (G-CSF) and interferons, depend on prior activation of components of the JAK/STAT signalling pathway. We report here that the myeloid cell line NFS-60 shows aberrant JAK/STAT signalling yet elicits expected biological responses to G-CSF and interferons-alpha/beta and gamma. Instead of increased phosphorylation of JAK1 and JAK2 in response to G-CSF and interferon-gamma, and JAK1 and Tyk2 in response to interferon-alpha/beta, we observed only an increase of phosphorylation of Tyk2 in response to all of these cytokines in NFS-60 cells. The subset of STAT proteins being activated in response to these cytokines was unusual as well. G-CSF activated STAT3 and STAT5A, whereas interferons activated, in addition to STAT1 and STAT5 other, as yet unidentified, DNA binding proteins. However, NFS-60 cells show normal biological responses to these cytokines, such as proliferation in response to G-CSF, and reduction of proliferation, induction of an anti-viral response and induction of specific genes in response to interferons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antiviral Agents / metabolism
  • Cell Division / drug effects
  • DNA-Binding Proteins / metabolism*
  • Gene Expression Regulation / drug effects
  • Granulocyte Colony-Stimulating Factor / pharmacology*
  • Interferon-alpha / pharmacology*
  • Interferon-beta / pharmacology*
  • Interferon-gamma / pharmacology*
  • Janus Kinase 3
  • Mice
  • Protein-Tyrosine Kinases / metabolism*
  • Proteins / metabolism
  • STAT1 Transcription Factor
  • Signal Transduction*
  • TYK2 Kinase
  • Trans-Activators / metabolism*
  • Tumor Cells, Cultured

Substances

  • Antiviral Agents
  • DNA-Binding Proteins
  • Interferon-alpha
  • Proteins
  • STAT1 Transcription Factor
  • Stat1 protein, mouse
  • Trans-Activators
  • Granulocyte Colony-Stimulating Factor
  • Interferon-beta
  • Interferon-gamma
  • Protein-Tyrosine Kinases
  • Jak3 protein, mouse
  • Janus Kinase 3
  • TYK2 Kinase
  • Tyk2 protein, mouse