ArticleThe Journal of biological chemistry2010
Regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) expression by interleukin-1 beta in pancreatic beta cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Melatonin Partially Attenuates Oxycodone-Induced Placental Stress Signaling and Fetal Brain Apoptosis in a Sex-Specific Manner.bioRxiv : the preprint server for biology · 2026Article
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- Enhancer of Zeste Homolog 2 (EZH2) Mediates Glucolipotoxicity-Induced Apoptosis in β-Cells.International journal of molecular sciences · 2020Article
- Article
- Inflammatory response in islet transplantation.International journal of endocrinology · 2014Review
- Sirtuin 3 regulates mouse pancreatic beta cell function and is suppressed in pancreatic islets isolated from human type 2 diabetic patients.Diabetologia · 2013Article
- Signalling danger: endoplasmic reticulum stress and the unfolded protein response in pancreatic islet inflammation.Diabetologia · 2013Review
- Article
- Is ARE/poly(U)-binding factor 1 (AUF1) a new player in cytokine-mediated beta cell apoptosis?Diabetologia · 2012Article
- Article
- The role of MafA in regulating cytokine expression in pancreatic beta cells.The Journal of biological chemistry · 2011Article
- Calcineurin/nuclear factor of activated T cells and MAPK signaling induce TNF-{alpha} gene expression in pancreatic islet endocrine cells.The Journal of biological chemistry · 2011Article
- Inhibition of deoxyhypusine synthase enhances islet {beta} cell function and survival in the setting of endoplasmic reticulum stress and type 2 diabetes.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis contributes to immune-mediated pancreatic beta cell destruction in type I diabetes. Exposure of beta cells to interleukin-1beta (IL-1beta) causes endoplasmic reticulum stress and activates proapoptotic networks. Here, we show that nuclear factor kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) signaling pathways regulate the expression of CCAAT/enhancer-binding protein homologous protein (CHOP), which mediates endoplasmic reticulum stress-induced apoptosis. Both CHOP mRNA and protein increase in beta cells treated with IL-1beta. In addition, prolonged exposure to high glucose further increases IL-1beta-triggered CHOP expression. IL-1beta also causes increased expression of C/EBP-beta and a reduction of MafA, NFATc2, and Pdx-1 expression in beta cells. Inhibition of the NF-kappaB and MAPK signaling pathways differentially attenuates CHOP expression. Knocking down CHOP by RNA interference protects beta cells from IL-1beta-induced apoptosis. These studies provide direct mechanistic links between cytokine-induced signaling pathways and CHOP-mediated apoptosis of beta cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.