Extracellular signal-regulated kinase is essential for interleukin-1-induced and nuclear factor kappaB-mediated gene expression in insulin-producing INS-1E cells

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The beta cell destruction and insulin deficiency that characterises type 1 diabetes mellitus is partially mediated by cytokines, such as IL-1beta, and by nitric oxide (NO)-dependent and -independent effector mechanisms. IL-1beta activates mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK), p38 and c-Jun NH2-terminal kinase (JNK), and the nuclear factor kappa B (NFkappaB) pathway. Both pathways are required for expression of the gene encoding inducible nitric oxide synthase (iNOS) and for IL-1beta-mediated beta cell death. The molecular mechanisms by which these two pathways regulate beta cell Nos2 expression are currently unknown. Therefore, the aim of this study was to clarify the putative crosstalk between MAPK and NFkappaB activation in beta cells.
Original languageEnglish
JournalDiabetologia
Volume48
Issue number12
Pages (from-to)2582-90
Number of pages9
ISSN0012-186X
DOIs
Publication statusPublished - 1 Dec 2005

    Research areas

  • Animals, Apoptosis, Blotting, Western, Cell Line, Tumor, Extracellular Signal-Regulated MAP Kinases, Flavonoids, Gene Expression, Humans, Imidazoles, Insulin, Insulin-Secreting Cells, Interleukin-1, MAP Kinase Kinase 4, Mitogen-Activated Protein Kinase Kinases, NF-kappa B, Nitric Oxide Synthase Type II, Phosphorylation, Pyridines, Rats, Serine, Synaptotagmin I, p38 Mitogen-Activated Protein Kinases

ID: 33902266