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

• Published in: FEBS letters Vol. 442; no. 1; pp. 57 - 60
• Main Authors: Morton, N M, de Groot, R P, Cawthorne, M A, Emilsson, V
• Format: Journal Article
• Language: English
• Published: England 08-01-1999
• Subjects: 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; Signal Transduction; STAT3 Transcription Factor; Trans-Activators - metabolism; Transfection
• ISSN: 0014-5793

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.