ArticleEMBO molecular medicine2013
Sustained expression of the transcription factor GLIS3 is required for normal beta cell function in adults.
Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 67 citations in OpenAlex.
- Identification of distinct functions of GLIS3 in β-cell generation critical to prevention of neonatal diabetes.bioRxiv : the preprint server for biology · 2026Article
- Glis3 as a critical regulator of Pit1-lineages and renal functions.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Alternative Splicing (AS) Provides an Alternative Mechanism for Regulating GLIS3 Expression and Activity.Cells · 2025Article
- A perfect islet: reviewing recent protocol developments and proposing strategies for stem cell derived functional pancreatic islets.Stem cell research & therapy · 2025Review
- A mechanism-informed deep neural network enables prioritization of regulators that drive cell state transitions.Nature communications · 2025Article
- Article
- eQTL mapping in fetal-like pancreatic progenitor cells reveals early developmental insights into diabetes risk.Nature communications · 2023Article
- Transcriptomic analysis of patients with clinical suspicion of maturity-onset diabetes of the young (MODY) with a negative genetic diagnosis.Orphanet journal of rare diseases · 2022Article
- Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells.Nature communications · 2021Article
- Neonatal diabetes mutations disrupt a chromatin pioneering function that activates the human insulin gene.Cell reports · 2021Article
- Transcription factor GLIS3: Critical roles in thyroid hormone biosynthesis, hypothyroidism, pancreatic beta cells and diabetes.Pharmacology & therapeutics · 2020Review
- Advances in Knowledge of Candidate Genes Acting at the Beta-Cell Level in the Pathogenesis of T1DM.Frontiers in endocrinology · 2020Review
- A GLIS3-CD133-WNT-signaling axis regulates the self-renewal of adult murine pancreatic progenitor-like cells in colonies and organoids.The Journal of biological chemistry · 2019Article
- Identification of placental genes linked to selective intrauterine growth restriction (IUGR) in dichorionic twin pregnancies: gene expression profiling study.Human genetics · 2019Article
- ATAC-seq reveals alterations in open chromatin in pancreatic islets from subjects with type 2 diabetes.Scientific reports · 2019Article
- GLIS1-3 transcription factors: critical roles in the regulation of multiple physiological processes and diseases.Cellular and molecular life sciences : CMLS · 2018Review
- Discovering human diabetes-risk gene function with genetics and physiological assays.Nature communications · 2018Article
- Discovery of a drug candidate for GLIS3-associated diabetes.Nature communications · 2018Article
- Loss of Glis3 causes dysregulation of retrotransposon silencing and germ cell demise in fetal mouse testis.Scientific reports · 2018Article
- Type 1 diabetes genome-wide association studies: not to be lost in translation.Clinical & translational immunology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Genome-wide association studies identified GLIS3 as a susceptibility locus for type 1 and type 2 diabetes. Global Glis3 deficiency in mice leads to congenital diabetes and neonatal lethality. In this study, we explore the role of Glis3 in adulthood using Glis3(+/-) and conditional knockout animals. We challenged Glis3(+/-) mice with high fat diet for 20 weeks and found that they developed diabetes because of impaired beta cell mass expansion. GLIS3 controls beta cell proliferation in response to high-fat feeding at least partly by regulating Ccnd2 transcription. To determine if sustained Glis3 expression is essential to normal beta cell function, we generated Glis3(fl/fl) /Pdx1Cre(ERT+) animal by intercrossing Glis3(fl/fl) mice with Pdx1Cre(ERT+) mice and used tamoxifen (TAM) to induce Glis3 deletion in adults. Adult Glis3(fl/fl) /Pdx1Cre(ERT+) mice are euglycaemic. TAM-mediated beta cell-specific inactivation of Glis3 in adult mice downregulates insulin expression, leading to hyperglycaemia and subsequently enhanced beta cell apoptosis. We conclude that normal Glis3 expression is required for pancreatic beta cell function and mass maintenance during adulthood, which impairment leads to diabetes in adults.
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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.