Interleukin-1β activates a short STAT-3 isoform in clonal insulin-secreting cells
Identifieur interne : 000B52 ( Main/Exploration ); précédent : 000B51; suivant : 000B53Interleukin-1β activates a short STAT-3 isoform in clonal insulin-secreting cells
Auteurs : Nicholas M. Morton [Royaume-Uni] ; Rolf P. De Groot [Pays-Bas] ; Michael A. Cawthorne [Royaume-Uni] ; Valur Emilsson [Royaume-Uni]Source :
- FEBS Letters [ 0014-5793 ] ; 1998.
Abstract
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.
Url:
DOI: 10.1016/S0014-5793(98)01623-8
Affiliations:
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<front><div type="abstract" xml:lang="en">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.</div>
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