Role of oxidative stress, endoplasmic reticulum stress, and c-Jun N-terminal kinase in pancreatic β-cell dysfunction and insulin resistance
- 31 August 2005
- journal article
- review article
- Published by Elsevier in The International Journal of Biochemistry & Cell Biology
- Vol. 37 (8) , 1595-1608
- https://doi.org/10.1016/j.biocel.2005.04.003
Abstract
No abstract availableKeywords
This publication has 96 references indexed in Scilit:
- β-cell neogenesis induced by adenovirus-mediated gene delivery of transcription factor pdx-1 into mouse pancreasGene Therapy, 2003
- Mitochondrial reactive oxygen species reduce insulin secretion by pancreatic β-cellsBiochemical and Biophysical Research Communications, 2002
- A central role for JNK in obesity and insulin resistanceNature, 2002
- Involvement of c-Jun N-terminal Kinase in Oxidative Stress-mediated Suppression of Insulin Gene ExpressionJournal of Biological Chemistry, 2002
- Diabetes Mellitus and Exocrine Pancreatic Dysfunction in Perk−/− Mice Reveals a Role for Translational Control in Secretory Cell SurvivalPublished by Elsevier ,2001
- In Vivo Protein Transduction: Delivery of a Biologically Active Protein into the MouseScience, 1999
- Transduction of full-length TAT fusion proteins into mammalian cells: TAT-p27Kip1 induces cell migrationNature Medicine, 1998
- Glycation-dependent, reactive oxygen species-mediated suppression of the insulin gene promoter activity in HIT cells.Journal of Clinical Investigation, 1997
- Purification and Characterization of a Novel Stress Protein, the 150-kDa Oxygen-regulated Protein (ORP150), from Cultured Rat Astrocytes and Its Expression in Ischemic Mouse BrainPublished by Elsevier ,1996
- Insulin-promoter-factor 1 is required for pancreas development in miceNature, 1994