Nitric oxide contributes to cytokine-induced apoptosis in pancreatic beta cells via potentiation of JNK activity and inhibition of Akt
Research output: Contribution to journal › Journal article › Research › peer-review
Pro-inflammatory cytokines cause beta cell secretory dysfunction and apoptosis--a process implicated in the pathogenesis of type 1 diabetes. Cytokines induce the expression of inducible nitric oxide (NO) synthase (iNOS) leading to NO production. NO contributes to cytokine-induced apoptosis, but the underlying mechanisms are unclear. The aim of this study was to investigate whether NO modulates signalling via mitogen-activated protein kinases (MAPKs) and Akt.
| Original language | English |
|---|---|
| Journal | Diabetologia |
| Volume | 48 |
| Issue number | 10 |
| Pages (from-to) | 2039-50 |
| Number of pages | 12 |
| ISSN | 0012-186X |
| DOIs | |
| Publication status | Published - 1 Oct 2005 |
- Animals, Apoptosis, Blotting, Western, Cell Separation, Cells, Cultured, Cytokines, Dose-Response Relationship, Drug, Enzyme Activation, Enzyme Inhibitors, Humans, Insulin, Insulin-Secreting Cells, MAP Kinase Kinase 4, Mice, Mitogen-Activated Protein Kinases, NG-Nitroarginine Methyl Ester, Nitric Oxide, Nitric Oxide Donors, Nitric Oxide Synthase Type II, Oncogene Protein v-akt, S-Nitroso-N-Acetylpenicillamine, Signal Transduction, p38 Mitogen-Activated Protein Kinases
Research areas
ID: 33902384