ArticleCell stem cell2019
Modeling Monogenic Diabetes using Human ESCs Reveals Developmental and Metabolic Deficiencies Caused by Mutations in HNF1A.
Article in Cell stem cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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Who cites it
61 citing papers in PubMed, 83 citations in OpenAlex.
- ProtectiveiScience · 2026Article
- Pancreatic organoids and organoid-on-a-chip platforms: from disease modeling to precision therapy.Journal of translational medicine · 2026Review
- Rethinking HNF1A-MODY: HNF1A at the crossroads of development and multiorgan metabolic disease.Genes & development · 2026Article
- Defective HNF1A hinders GLI3 processing favoring duodenal versus pancreatic fate, thus leading to intestinal elongation in vivo.Genes & development · 2026Article
- Article
- Patient-derived induced pluripotent stem cells for precision modelling of monogenic beta cell disorders.Frontiers in endocrinology · 2026Review
- HNF1α-Q125ter-mediated mitochondrial dysfunction and impaired mitophagy in β-cells.Journal of molecular endocrinology · 2025Article
- Bridging pancreatic and hepatic development: overlapping genes and their role in diabetes.Cellular & molecular biology letters · 2025Review
- HNF1A and A1CF coordinate a beta cell transcription-splicing axis that is disrupted in type 2 diabetes.Cell metabolism · 2025Article
- Modeling Genetic Risk of β-Cell Dysfunction in Human Induced Pluripotent Stem Cells From Patients Carrying the MTNR1B Risk Variant.Journal of pineal research · 2025Article
- Efficient cytoplasmic cell quantification using a semi-automated FIJI-based tool.Scientific reports · 2025Article
- Type 2 diabetes mellitus - conventional therapies and future perspectives in innovative treatment.Biochemistry and biophysics reports · 2025Review
- ZHX3 interacts with CEBPB to repress hepatic gluconeogenic gene expression and uric acid secretion.PNAS nexus · 2025Article
- The perfect storm: unraveling the interplay of genetic predisposition and viral triggers in type 1 diabetes pathogenesis.Frontiers in endocrinology · 2025Review
- Investigating the pathogenicity of the recessivemedRxiv : the preprint server for health sciences · 2024Article
- Generation of a fluorescent mNeonGreen insulin reporter line in the H1 (WA01) hESC background.Stem cell research · 2024Article
- Recent progress in modeling and treating diabetes using stem cell-derived islets.Stem cells translational medicine · 2024Review
- From iPSCs to Pancreatic β Cells: Unveiling Molecular Pathways and Enhancements with Vitamin C and Retinoic Acid in Diabetes Research.International journal of molecular sciences · 2024Article
- Identification of unique cell type responses in pancreatic islets to stress.Nature communications · 2024Article
- Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
Abstract
Human monogenic diabetes, caused by mutations in genes involved in beta cell development and function, has been a challenge to study because multiple mouse models have not fully recapitulated the human disease. Here, we use genome edited human embryonic stem cells to understand the most common form of monogenic diabetes, MODY3, caused by mutations in the transcription factor HNF1A. We found that HNF1A is necessary to repress an alpha cell gene expression signature, maintain endocrine cell function, and regulate cellular metabolism. In addition, we identified the human-specific long non-coding RNA, LINKA, as an HNF1A target necessary for normal mitochondrial respiration. These findings provide a possible explanation for the species difference in disease phenotypes observed with HNF1A mutations and offer mechanistic insights into how the HNF1A gene may also influence type 2 diabetes.
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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 Socratic graph.