ArticleDiabetes2009
Methyltransferase Set7/9 maintains transcription and euchromatin structure at islet-enriched genes.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis 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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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Roles of Epigenetic Modifications in the Differentiation and Function of Pancreatic β-Cells.Frontiers in cell and developmental biology · 2020Pooled it
- The role of epigenetic signatures in type 2 diabetes: therapeutic advances and lifestyle interventions.Acta diabetologica · 2026Review
- Emerging Roles of Post-Translational Modifications in Metabolic Homeostasis and Type 2 Diabetes.International journal of molecular sciences · 2025Review
- Histone Methylation, Energy Metabolism, and Alzheimer's Disease.Aging and disease · 2024Review
- Lysine-specific methyltransferase Set7/9 in stemness, differentiation, and development.Biology direct · 2024Review
- Article
- Methylation of histone H3 lysine 4 is required for maintenance of beta cell function in adult mice.Diabetologia · 2023Article
- Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.International journal of biological sciences · 2023Review
- How Protein Methylation Regulates Steroid Receptor Function.Endocrine reviews · 2022Review
- PDX1 is the cornerstone of pancreatic β-cell functions and identity.Frontiers in molecular biosciences · 2022Review
- Oxidative stress-mediated beta cell death and dysfunction as a target for diabetes management.Frontiers in endocrinology · 2022Review
- SetD7 (Set7/9) is a novel target of PPARγ that promotes the adaptive pancreatic β-cell glycemic response.The Journal of biological chemistry · 2021Article
- Epigenetic Regulation of PDX-1 in Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Epigenetic Regulation of β Cell Identity and Dysfunction.Frontiers in endocrinology · 2021Review
- Epigenetics in β-cell adaptation and type 2 diabetes.Current opinion in pharmacology · 2020Review
- SET7/9 promotes multiple malignant processes in breast cancer development via RUNX2 activation and is negatively regulated by TRIM21.Cell death & disease · 2020Article
- An overview on small molecule-induced differentiation of mesenchymal stem cells into beta cells for diabetic therapy.Stem cell research & therapy · 2019Review
- LIM-domain transcription complexes interact with ring-finger ubiquitin ligases and thereby impact islet β-cell function.The Journal of biological chemistry · 2019Article
- The Lysine Demethylase KDM5B Regulates Islet Function and Glucose Homeostasis.Journal of diabetes research · 2019Article
- Revealing inhibition difference between PFI-2 enantiomers against SETD7 by molecular dynamics simulations, binding free energy calculations and unbinding pathway analysis.Scientific reports · 2017Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveThe activation of beta-cell genes, particularly of those encoding preproinsulin, requires an appropriate euchromatin (or "open") DNA template characterized by hypermethylation of Lys4 of histone H3. We hypothesized that this modification is maintained in islet beta-cells by the action of the histone methyltransferase Set7/9. RESEARCH DESIGN AND
methodsTo identify the role of Set7/9, we characterized its expression pattern and gene regulation and studied its function using RNA interference in both cell lines and primary mouse islets.
resultsWithin the pancreas, Set7/9 protein shows striking specificity for islet cells, including alpha- and beta-cells, as well as occasional cells within ducts. Consistent with these findings, the Set7/9 gene promoter contained an islet-specific enhancer located between -5,768 and -6,030 base pairs (relative to the transcriptional start site) that exhibited Pdx1-responsive activation in beta-cells. To study Set7/9 function, we depleted insulinoma cells and primary mouse islets of Set7/9 protein using siRNA. Following siRNA treatment, we observed striking repression of genes involved in glucose-stimulated insulin secretion, including Ins1/2, Glut2, and MafA. These changes in transcription were accompanied by loss of dimethylated H3 Lys4 and RNA polymerase II recruitment, particularly at the Ins1/2 and Glut2 genes. Consistent with these data, depletion of Set7/9 in islets led to defects in glucose-stimulated Ca(2+) mobilization and insulin secretion.
conclusionsWe conclude that Set7/9 is required for normal beta-cell function, likely through the maintenance of euchromatin structure at genes necessary for glucose-stimulated insulin secretion.
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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.