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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Extracellular signal-regulated kinase is essential for interleukin-1-induced and nuclear factor kappaB-mediated gene expression in insulin-producing INS-1E cells. / Larsen, Lykke; Størling, J; Darville, M; Eizirik, D L; Bonny, C; Billestrup, N; Mandrup-Poulsen, Thomas.
I: Diabetologia, Bind 48, Nr. 12, 01.12.2005, s. 2582-90.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › fagfællebedømt
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TY - JOUR
T1 - Extracellular signal-regulated kinase is essential for interleukin-1-induced and nuclear factor kappaB-mediated gene expression in insulin-producing INS-1E cells
AU - Larsen, Lykke
AU - Størling, J
AU - Darville, M
AU - Eizirik, D L
AU - Bonny, C
AU - Billestrup, N
AU - Mandrup-Poulsen, Thomas
PY - 2005/12/1
Y1 - 2005/12/1
N2 - 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.
AB - 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.
KW - Animals
KW - Apoptosis
KW - Blotting, Western
KW - Cell Line, Tumor
KW - Extracellular Signal-Regulated MAP Kinases
KW - Flavonoids
KW - Gene Expression
KW - Humans
KW - Imidazoles
KW - Insulin
KW - Insulin-Secreting Cells
KW - Interleukin-1
KW - MAP Kinase Kinase 4
KW - Mitogen-Activated Protein Kinase Kinases
KW - NF-kappa B
KW - Nitric Oxide Synthase Type II
KW - Phosphorylation
KW - Pyridines
KW - Rats
KW - Serine
KW - Synaptotagmin I
KW - p38 Mitogen-Activated Protein Kinases
U2 - 10.1007/s00125-005-0039-9
DO - 10.1007/s00125-005-0039-9
M3 - Journal article
C2 - 16283237
VL - 48
SP - 2582
EP - 2590
JO - Diabetologia
JF - Diabetologia
SN - 0012-186X
IS - 12
ER -
ID: 33902266