ArticleThe Journal of clinical investigation2013
Inactivation of specific β cell transcription factors in type 2 diabetes.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 328 papers, 1 of them a synthesis that pooled it.
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Who cites it
328 citing papers in PubMed, 1 synthesis or guideline pooled it, 508 citations in OpenAlex.
- Insulin gene mutations and posttranslational and translocation defects: associations with diabetes.Endocrine · 2020Pooled it
- Genetic background modulates MafADiabetologia · 2026Article
- Adipocyte-derived exosomal ANGPTL2 promotes beta cell dysfunction via the EIF2α/ATF4/CHOP stress pathway in mice.Diabetologia · 2026Article
- Human β-Cell Dedifferentiation and Diabetes.Journal of diabetes · 2026Review
- Dual Modulation of Prostaglandin E2 Receptors EP3 and EP4 Protects β-Cell Mass in a Model of Aggressive Autoimmune Inflammation.Diabetes · 2026Article
- Diabetes-associated MYT1 and ST18 genes regulate human beta cell insulin secretion and survival via other diabetes risk genes.Diabetologia · 2026Article
- Nardilysin regulatesBiochemistry and biophysics reports · 2026Article
- Polystyrene Nanoplastics Drive β-Cell Dedifferentiation Through Dendritic Cell-Intrinsic MHC-I-Dependent Inflammatory Crosstalk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MAFB in Pancreatic β-Cell Development and Dysfunction: Implications for Diabetes and Translational Applications.Biomolecules · 2026Review
- Review
- Pancreatic β-cell aging in physiology and diabetes: emerging roles of m6A mRNA methylation.Journal of molecular endocrinology · 2026Review
- QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Workload-induced changes to cell state contribute to β-cell failure in diabetes.bioRxiv : the preprint server for biology · 2026Article
- The molecular mechanisms of incretin resistance in Type 2 Diabetes Mellitus (T2DM).Nutrition & diabetes · 2026Review
- Zinc accumulation-induced integrated stress response triggers β-cell identity loss.Cell research · 2026Article
- Stimulation to secrete insulin induces pancreatic β-cell dysfunction through Tfe3 activation.iScience · 2026Article
- An atlas of genetic effects on the monocyte methylome across European and African populations.Genome medicine · 2026Article
- Single-cell RNA-seq and in vitro study reveal Fusobacterium nucleatum impairs β-cell identity in type 2 diabetes via the NF-κB-CDKN1C axis.Journal of translational medicine · 2026Article
- Review
- Human donor islets coated with functionalized chitosan and alginate nanoscale layers can restore normoglycemia in diabetic mice.Materials today. Bio · 2026Article
268 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Type 2 diabetes (T2DM) commonly arises from islet β cell failure and insulin resistance. Here, we examined the sensitivity of key islet-enriched transcription factors to oxidative stress, a condition associated with β cell dysfunction in both type 1 diabetes (T1DM) and T2DM. Hydrogen peroxide treatment of β cell lines induced cytoplasmic translocation of MAFA and NKX6.1. In parallel, the ability of nuclear PDX1 to bind endogenous target gene promoters was also dramatically reduced, whereas the activity of other key β cell transcriptional regulators was unaffected. MAFA levels were reduced, followed by a reduction in NKX6.1 upon development of hyperglycemia in db/db mice, a T2DM model. Transgenic expression of the glutathione peroxidase-1 antioxidant enzyme (GPX1) in db/db islet β cells restored nuclear MAFA, nuclear NKX6.1, and β cell function in vivo. Notably, the selective decrease in MAFA, NKX6.1, and PDX1 expression was found in human T2DM islets. MAFB, a MAFA-related transcription factor expressed in human β cells, was also severely compromised. We propose that MAFA, MAFB, NKX6.1, and PDX1 activity provides a gauge of islet β cell function, with loss of MAFA (and/or MAFB) representing an early indicator of β cell inactivity and the subsequent deficit of more impactful NKX6.1 (and/or PDX1) resulting in overt dysfunction associated with T2DM.
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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.