ArticleThe Journal of biological chemistry2014
A combined "omics" approach identifies N-Myc interactor as a novel cytokine-induced regulator of IRE1 protein and c-Jun N-terminal kinase in pancreatic beta cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Rapid protein carbonylation and decreased insulin secretion induced by inflammatory oxidative stress compounds.Free radical biology & medicine · 2026Article
- Review
- IRE1/XBP1 and endoplasmic reticulum signaling - from basic to translational research for cardiovascular disease.Current opinion in physiology · 2022Article
- The Pancreatic ß-cell Response to Secretory Demands and Adaption to Stress.Endocrinology · 2021Review
- Early Cytokine-Induced Transient NOX2 Activity Is ER Stress-Dependent and Impacts β-Cell Function and Survival.Antioxidants (Basel, Switzerland) · 2021Article
- Inositol Requiring Enzyme (IRE), a multiplayer in sensing endoplasmic reticulum stress.Animal cells and systems · 2021Review
- Pathological β-Cell Endoplasmic Reticulum Stress in Type 2 Diabetes: Current Evidence.Frontiers in endocrinology · 2021Review
- YIPF5 mutations cause neonatal diabetes and microcephaly through endoplasmic reticulum stress.The Journal of clinical investigation · 2020Article
- Endoplasmic Reticulum Protein Quality Control in β Cells.Seminars in cell & developmental biology · 2020Review
- Pancreatic β-cells in type 1 and type 2 diabetes mellitus: different pathways to failure.Nature reviews. Endocrinology · 2020Review
- Review
- N-myc and STAT interactor correlates with severity and prognosis in acute-on-chronic liver failure of hepatitis B virus.Journal of gastroenterology and hepatology · 2019Article
- MicroRNA-24 promotes pancreatic beta cells toward dedifferentiation to avoid endoplasmic reticulum stress-induced apoptosis.Journal of molecular cell biology · 2019Article
- ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis.Oxidative medicine and cellular longevity · 2019Review
- Dual Role of Nitric Oxide in Regulating the Response of β Cells to DNA Damage.Antioxidants & redox signaling · 2018Review
- Imaging of Human Insulin Secreting Cells with Gd-DOTA-P88, a Paramagnetic Contrast Agent Targeting the Beta Cell Biomarker FXYD2γa.Molecules (Basel, Switzerland) · 2018Article
- A nanobody-based tracer targeting DPP6 for non-invasive imaging of human pancreatic endocrine cells.Scientific reports · 2017Article
- Article
- Glial cell-line derived neurotrophic factor protects human islets from nutrient deprivation and endoplasmic reticulum stress induced apoptosis.Scientific reports · 2017Article
- Proteome-scale Binary Interactomics in Human Cells.Molecular & cellular proteomics : MCP · 2016Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes is an autoimmune disease with a strong inflammatory component. The cytokines interleukin-1β and interferon-γ contribute to beta cell apoptosis in type 1 diabetes. These cytokines induce endoplasmic reticulum stress and the unfolded protein response (UPR), contributing to the loss of beta cells. IRE1α, one of the UPR mediators, triggers insulin degradation and inflammation in beta cells and is critical for the transition from "physiological" to "pathological" UPR. The mechanisms regulating inositol-requiring protein 1α (IRE1α) activation and its signaling for beta cell "adaptation," "stress response," or "apoptosis" remain to be clarified. To address these questions, we combined mammalian protein-protein interaction trap-based IRE1α interactome and functional genomic analysis of human and rodent beta cells exposed to pro-inflammatory cytokines to identify novel cytokine-induced regulators of IRE1α. Based on this approach, we identified N-Myc interactor (NMI) as an IRE1α-interacting/modulator protein in rodent and human pancreatic beta cells. An increased expression of NMI was detected in islets from nonobese diabetic mice with insulitis and in rodent or human beta cells exposed in vitro to the pro-inflammatory cytokines interleukin-1β and interferon-γ. Detailed mechanistic studies demonstrated that NMI negatively modulates IRE1α-dependent activation of JNK and apoptosis in rodent and human pancreatic beta cells. In conclusion, by using a combined omics approach, we identified NMI induction as a novel negative feedback mechanism that decreases IRE1α-dependent activation of JNK and apoptosis in cytokine-exposed beta cells
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