ArticleMolecular and cellular biology2009
Transcription factor Glis3, a novel critical player in the regulation of pancreatic beta-cell development and insulin gene expression.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 105 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
105 citing papers in PubMed, 3 syntheses or guidelines pooled it, 150 citations in OpenAlex.
- Genome-wide association meta-analysis identifies two novel loci associated with dental caries.BMC oral health · 2024Pooled it
- Systematic evaluation of validated type 2 diabetes and glycaemic trait loci for association with insulin clearance.Diabetologia · 2013Pooled it
- Meta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians.Nature genetics · 2011Pooled it
- A Novel Renal Manifestation inJournal of medical cases · 2026Article
- 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
- Distinct Roles of Common Genetic Variants and Their Contributions to Diabetes: MODY and Uncontrolled T2DM.Biomolecules · 2025Review
- A mechanism-informed deep neural network enables prioritization of regulators that drive cell state transitions.Nature communications · 2025Article
- Post translational modification regulation of transcription factors governing pancreatic β-cell identity and functional mass.Frontiers in endocrinology · 2025Review
- Article
- Review
- Consistent cord blood DNA methylation signatures of gestational age between South Asian and white European cohorts.Clinical epigenetics · 2024Article
- GLIS3 expression in the thyroid gland in relation to TSH signaling and regulation of gene expression.Cellular and molecular life sciences : CMLS · 2024Article
- An Insight into Vital Genes Responsible for β-cell Formation.Advances in experimental medicine and biology · 2024Article
- eQTL mapping in fetal-like pancreatic progenitor cells reveals early developmental insights into diabetes risk.Nature communications · 2023Article
- Deciphering early human pancreas development at the single-cell level.Nature communications · 2023Article
- Characterization of cell-fate decision landscapes by estimating transcription factor dynamics.Cell reports methods · 2023Article
- Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedPierreux, Christophe E [added]; Lemaigre, Frederic P [added]
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
In this study, we report that the Krüppel-like zinc finger transcription factor Gli-similar 3 (Glis3) is induced during the secondary transition of pancreatic development, a stage of cell lineage specification and extensive patterning, and that Glis3(zf/zf) mutant mice develop neonatal diabetes, evidenced by hyperglycemia and hypoinsulinemia. The Glis3(zf/zf) mutant mouse pancreas shows a dramatic loss of beta and delta cells, contrasting a smaller relative loss of alpha, PP, and epsilon cells. In addition, Glis3(zf/zf) mutant mice develop ductal cysts, while no significant changes were observed in acini. Gene expression profiling and immunofluorescent staining demonstrated that the expression of pancreatic hormones and several transcription factors important in endocrine cell development, including Ngn3, MafA, and Pdx1, were significantly decreased in the developing pancreata of Glis3(zf/zf) mutant mice. The population of pancreatic progenitors appears not to be greatly affected in Glis3(zf/zf) mutant mice; however, the number of neurogenin 3 (Ngn3)-positive endocrine cell progenitors is significantly reduced. Our study indicates that Glis3 plays a key role in cell lineage specification, particularly in the development of mature pancreatic beta cells. In addition, we provide evidence that Glis3 regulates insulin gene expression through two Glis-binding sites in its proximal promoter, indicating that Glis3 also regulates beta-cell function.
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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.