ArticleDiabetologia2014
Dyrk1a haploinsufficiency induces diabetes in mice through decreased pancreatic beta cell mass.
Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Emerging role of DYRK1A as a target in cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Gene Expression Studies in Down Syndrome: What Do They Tell Us about Disease Phenotypes?International journal of molecular sciences · 2024Review
- Modelling human diabetesFrontiers in endocrinology · 2024Review
- New insights into the roles for DYRK family in mammalian development and congenital diseases.Genes & diseases · 2023Review
- Article
- Inhibition of DYRK1a Enhances Cardiomyocyte Cycling After Myocardial Infarction.Circulation research · 2022Article
- Article
- Diabetic Kinome Inhibitors-A New Opportunity for β-Cells Restoration.International journal of molecular sciences · 2021Review
- Data supporting a pilot high-throughput screen of a drug library for identification of DYRK1A inhibitors and high-content imaging analysis of identified harmine analogs.Data in brief · 2021Article
- New Aspects of Diabetes Research and Therapeutic Development.Pharmacological reviews · 2021Review
- Identification of harmine and β-carboline analogs from a high-throughput screen of an approved drug collection; profiling as differential inhibitors of DYRK1A and monoamine oxidase A and for in vitro and in vivo anti-cancer studies.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2021Article
- Scientific Advances in Diabetes: The Impact of the Innovative Medicines Initiative.Frontiers in medicine · 2021Review
- Down Syndrome Is a Metabolic Disease: Altered Insulin Signaling Mediates Peripheral and Brain Dysfunctions.Frontiers in neuroscience · 2020Review
- Dual-specificity tyrosine phosphorylation-regulated kinase 1A ameliorates insulin resistance in neurons by up-regulating IRS-1 expression.The Journal of biological chemistry · 2019Article
- CC-401 Promotes β-Cell Replication via Pleiotropic Consequences of DYRK1A/B Inhibition.Endocrinology · 2018Article
- The phosphorylation status of T522 modulates tissue-specific functions of SIRT1 in energy metabolism in mice.EMBO reports · 2017Article
- Development of a reliable automated screening system to identify small molecules and biologics that promote human β-cell regeneration.American journal of physiology. Endocrinology and metabolism · 2016Article
- Novel factors modulating human β-cell proliferation.Diabetes, obesity & metabolism · 2016Review
- Inhibition of DYRK1A Stimulates Human β-Cell Proliferation.Diabetes · 2016Article
- DYRK1A haploinsufficiency causes a new recognizable syndrome with microcephaly, intellectual disability, speech impairment, and distinct facies.European journal of human genetics : EJHG · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisGrowth factors and nutrients are important regulators of pancreatic beta cell mass and function. However, the signalling pathways by which these factors modulate these processes have not yet been fully elucidated. DYRK1A (also named minibrain/MNB) is a member of the dual-specificity tyrosine phosphorylation-regulated kinase (DYRK) family that has been conserved across evolution. A significant amount of data implicates DYRK1A in brain growth and function, as well as in neurodegenerative processes in Alzheimer's disease and Down's syndrome. We investigated here whether DYRK1A would be an attractive candidate for beta cell growth modulation.
methodsTo study the role of DYRK1A in beta cell growth, we used Dyrk1a-deficient mice.
resultsWe show that DYRK1A is expressed in pancreatic islets and provide evidence that changes in Dyrk1a gene dosage in mice strongly modulate glycaemia and circulating insulin levels. Specifically, Dyrk1a-haploinsufficient mice show severe glucose intolerance, reduced beta cell mass and decreased beta cell proliferation. CONCLUSIONS/
interpretationTaken together, our data indicate that DYRK1A is a critical kinase for beta cell growth as Dyrk1a-haploinsufficient mice show a diabetic profile.
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