ArticleJournal of diabetes research2019
The Lysine Demethylase KDM5B Regulates Islet Function and Glucose Homeostasis.
Article in Journal of diabetes research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Single-cell RNA sequencing in diabetic foot ulcers: pathogenesis, biomarkers, and translational potential.Frontiers in clinical diabetes and healthcare · 2026Review
- Harnessing Pharmacomultiomics for Precision Medicine in Diabetes: A Comprehensive Review.Biomedicines · 2025Review
- DeepAnnotation: A novel interpretable deep learning-based genomic selection model that integrates comprehensive functional annotations.GigaScience · 2025Article
- Integrating GWAS and machine learning for disease risk prediction in the Taiwanese Hakka population.Frontiers in genetics · 2025Article
- AUP1 transcriptionally activated by KDM5B reprograms lipid metabolism to promote the malignant progression of cervical cancer.International journal of oncology · 2024Article
- Roles of Lysine Methylation in Glucose and Lipid Metabolism: Functions, Regulatory Mechanisms, and Therapeutic Implications.Biomolecules · 2024Review
- Histone methylation: at the crossroad between circadian rhythms in transcription and metabolism.Frontiers in genetics · 2024Review
- Epigenetic Regulation of Pancreas Development and Function.Advances in anatomy, embryology, and cell biology · 2024Review
- A multi-layered network model identifies Akt1 as a common modulator of neurodegeneration.Molecular systems biology · 2023Article
- PICK1-Deficient Mice Maintain Their Glucose Tolerance During Diet-Induced Obesity.Journal of the Endocrine Society · 2023Article
- Histone demethylase KDM5B licenses macrophage-mediated inflammatory responses by repressing Nfkbia transcription.Cell death and differentiation · 2023Article
- The mActa diabetologica · 2023Article
- Survivin promotes a glycolytic switch in CD4iScience · 2022Article
- Pharmacoepigenetics in type 2 diabetes: is it clinically relevant?Diabetologia · 2022Article
- Histone Methylation Related Therapeutic Challenge in Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- Epigenetics and Beyond: Targeting Histone Methylation to Treat Type 2 Diabetes Mellitus.Frontiers in pharmacology · 2021Review
- KDM4B facilitates colorectal cancer growth and glucose metabolism by stimulating TRAF6-mediated AKT activation.Journal of experimental & clinical cancer research : CR · 2020Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsPosttranslational modifications of histones and transcription factors regulate gene expression and are implicated in beta-cell failure and diabetes. We have recently shown that preserving H3K27 and H3K4 methylation using the lysine demethylase inhibitor GSK-J4 reduces cytokine-induced destruction of beta-cells and improves beta-cell function. Here, we investigate the therapeutic potential of GSK-J4 to prevent diabetes development and examine the importance of H3K4 methylation for islet function. MATERIALS AND
methodsWe used two mouse models of diabetes to investigate the therapeutic potential of GSK-J4. To clarify the importance of H3K4 methylation, we characterized a mouse strain with knockout (KO) of the H3K4 demethylase KDM5B.
resultsGSK-J4 administration failed to prevent the development of experimental diabetes induced by multiple low-dose streptozotocin or adoptive transfer of splenocytes from acutely diabetic NOD to NODscid mice. KDM5B-KO mice were growth retarded with altered body composition, had low IGF-1 levels, and exhibited reduced insulin secretion. Interestingly, despite secreting less insulin, KDM5B-KO mice were able to maintain normoglycemia following oral glucose tolerance test, likely via improved insulin sensitivity, as suggested by insulin tolerance testing and phosphorylation of proteins belonging to the insulin signaling pathway. When challenged with high-fat diet, KDM5B-deficient mice displayed similar weight gain and insulin sensitivity as wild-type mice.
conclusionOur results show a novel role of KDM5B in metabolism, as KDM5B-KO mice display growth retardation and improved insulin sensitivity.
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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.