ArticleProceedings of the National Academy of Sciences of the United States of America2007
Differential regulation of CHOP-10/GADD153 gene expression by MAPK signaling in pancreatic beta-cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Transcriptomic analysis of cellular senescence induced by ectopic expression of ATF6α in human breast cancer cells.PloS one · 2024Article
- Identification of 1,2,3-triazole derivatives that protect pancreatic β cells against endoplasmic reticulum stress-mediated dysfunction and death through the inhibition of C/EBP-homologous protein expression.Bioorganic & medicinal chemistry · 2016Article
- Selective and sequential loss of transcriptional factors: A hallmark of β-cell failure in type 2 diabetes?Journal of diabetes investigation · 2014Article
- Glucokinase activation ameliorates ER stress-induced apoptosis in pancreatic β-cells.Diabetes · 2013Article
- Article
- IFN-α and lipopolysaccharide upregulate APOBEC3 mRNA through different signaling pathways.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- DNA methylation profiling identifies epigenetic dysregulation in pancreatic islets from type 2 diabetic patients.The EMBO journal · 2012Article
- 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
- ERK/ribosomal S6 kinase (RSK) signaling positively regulates death receptor 5 expression through co-activation of CHOP and Elk1.The Journal of biological chemistry · 2010Article
- Regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) expression by interleukin-1 beta in pancreatic beta cells.The Journal of biological chemistry · 2010Article
- GLP-1 mediates antiapoptotic effect by phosphorylating Bad through a beta-arrestin 1-mediated ERK1/2 activation in pancreatic beta-cells.The Journal of biological chemistry · 2010Article
- Oligonucleotide microarray analysis of apoptosis induced by 15-methoxypinusolidic acid in microglial BV2 cells.British journal of pharmacology · 2009Article
- Sumoylation regulates the transcriptional activity of MafA in pancreatic beta cells.The Journal of biological chemistry · 2009Article
- Mouse pancreatic islets are resistant to indoleamine 2,3 dioxygenase-induced general control nonderepressible-2 kinase stress pathway and maintain normal viability and function.The American journal of pathology · 2009Article
- Chromatin-bound mitogen-activated protein kinases transmit dynamic signals in transcription complexes in beta-cells.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- MafA is a dedicated activator of the insulin gene in vivo.The Journal of endocrinology · 2008Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
CHOP-10 (GADD153/DDIT-3) is a bZIP protein involved in differentiation and apoptosis. Its expression is induced in response to stresses such as nutrient deprivation, perturbation of the endoplasmic reticulum, redox imbalance, and UV exposure. Here we show that CHOP expression is induced in cultured pancreatic beta-cells maintained in a basal glucose concentration of 5.5 mM and repressed by stimulatory glucose (>or=11 mM). Both induction and repression of CHOP are dependent on the MAPKs ERK1 and ERK2. Two regulatory composite sites containing overlapping MafA response elements (MARE) and CAAT enhancer binding (CEB) elements regulate transcription in an ERK1/2-dependent manner. One site (MARE-CEB), from -320 to -300 bp in the promoter, represses transcription. The other site (CEB-MARE), from +2,628 to +2,641 bp in the first intron of the CHOP gene, activates it. MafA can influence transcription of both sites. The MARE-CEB is repressed by MafA, whereas the CEB-MARE site, which is homologous to the A2C1 component of the glucose-sensitive RIPE3b region of the insulin gene promoter, is activated by MafA. These results indicate that ERK1/2 have dual roles in regulating CHOP gene expression via both promoter and intronic regions, depending on environmental and metabolic stresses imposed on pancreatic beta-cells.
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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.