Interleukin-1beta activates a short STAT-3 isoform in clonal insulin-secreting cells

FEBS Lett. 1999 Jan 8;442(1):57-60. doi: 10.1016/s0014-5793(98)01623-8.

Abstract

Interleukin-1beta (IL-1beta) is a potent inflammatory cytokine involved in type 1 diabetes and acts through defined IL-1beta signaling pathways. In the present work we describe induction of DNA binding activity to signal transducer and activator of transcription (STAT) in response to IL-1beta in clonal insulin-secreting cells. Moreover, IL-1beta activates a short isoform of STAT-3 that potently stimulates transcription. Immunoprecipitation studies reveal an interaction between the activated STAT-3 and the IL-1 receptor accessory protein indicating an association between the two signaling pathways. This may be a novel point of transduction cross talk and an additional mechanism utilised by IL-1beta in the pancreatic beta-cell during the process of type 1 diabetes.

MeSH terms

  • Base Sequence
  • Clone Cells
  • DNA / genetics
  • DNA / metabolism
  • DNA-Binding Proteins / metabolism*
  • Humans
  • Insulin / metabolism*
  • Insulin Secretion
  • Interleukin-1 / metabolism
  • Interleukin-1 / pharmacology*
  • Interleukin-1 Receptor Accessory Protein
  • Islets of Langerhans / cytology
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / physiology
  • Protein Binding
  • Proteins / metabolism
  • Receptors, Interleukin-1 / metabolism
  • STAT3 Transcription Factor
  • Signal Transduction
  • Trans-Activators / metabolism*
  • Transfection

Substances

  • DNA-Binding Proteins
  • IL1RAP protein, human
  • Insulin
  • Interleukin-1
  • Interleukin-1 Receptor Accessory Protein
  • Proteins
  • Receptors, Interleukin-1
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Trans-Activators
  • DNA