Growth arrest- and DNA-damage-inducible 45beta gene inhibits c-Jun N-terminal kinase and extracellular signal-regulated kinase and decreases IL-1beta-induced apoptosis in insulin-producing INS-1E cells

Research output: Contribution to journalJournal articleResearchpeer-review

IL-1beta is a candidate mediator of apoptotic beta cell destruction, a process that leads to type 1 diabetes and progression of type 2 diabetes. IL-1beta activates beta cell c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38, all of which are members of the mitogen-activated protein kinase (MAPK) family. Inhibition of JNK prevents IL-1beta-mediated beta cell destruction. In mouse embryo fibroblasts and 3DO T cells, overexpression of the gene encoding growth arrest and DNA-damage-inducible 45beta (Gadd45b) downregulates pro-apoptotic JNK signalling. The aim of this study was to investigate if Gadd45b prevents IL-1beta-induced beta cell MAPK signalling and apoptosis.
Original languageEnglish
JournalDiabetologia
Volume49
Issue number5
Pages (from-to)980-9
Number of pages10
ISSN0012-186X
DOIs
Publication statusPublished - 1 May 2006

    Research areas

  • 3T3 Cells, Animals, Antigens, Differentiation, Apoptosis, Cell Division, DNA Damage, DNA Primers, Extracellular Signal-Regulated MAP Kinases, Gene Expression Regulation, Neoplastic, Insulin, Insulinoma, Interleukin-1, JNK Mitogen-Activated Protein Kinases, Mice, Pancreatic Neoplasms, Rats, Reverse Transcriptase Polymerase Chain Reaction, Transfection

ID: 33902165