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Interleukin‐1β activates a short STAT‐3 isoform in clonal insulin‐secreting cells
Author(s) -
Morton Nicholas M.,
de Groot Rolf P.,
Cawthorne Michael A.,
Emilsson Valur
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01623-8
Subject(s) - stat , stat protein , signal transduction , microbiology and biotechnology , gene isoform , cytokine , biology , transcription factor , jak stat signaling pathway , chemistry , stat3 , immunology , biochemistry , gene , tyrosine kinase
Interleukin‐1β (IL‐1β) is a potent inflammatory cytokine involved in type 1 diabetes and acts through defined IL‐1β 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‐1β in clonal insulin‐secreting cells. Moreover, IL‐1β 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‐1β in the pancreatic β‐cell during the process of type 1 diabetes.