ArticleIslets2015
Aurora Kinase A is critical for the Nkx6.1 mediated β-cell proliferation pathway.
Article in Islets, 2015. 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, 29 citations in OpenAlex.
- Nr4a1 β-cell specific deletion impairs glucose tolerance in female mice.American journal of physiology. Endocrinology and metabolism · 2026Article
- Article
- Bioavailable Microbial Metabolites of Flavanols Demonstrate Highly Individualized Bioactivity on In Vitro β-Cell Functions Critical for Metabolic Health.Metabolites · 2023Article
- Functional, metabolic and transcriptional maturation of human pancreatic islets derived from stem cells.Nature biotechnology · 2022Article
- Decreased proliferation of aged rat beta cells corresponds with enhanced expression of the cell cycle inhibitor p27Biology of the cell · 2021Article
- Transcriptome analysis of arterial and venous circulating miRNAs during hypertension.Scientific reports · 2021Article
- Inhibition of Aurora-A improves insulin resistance by ameliorating islet inflammation and controlling interleukin-6 in a diabetic mouse model.Adipocyte · 2020Article
- NKX6.1 transcription factor: a crucial regulator of pancreatic β cell development, identity, and proliferation.Stem cell research & therapy · 2020Review
- Treatment with Mammalian Ste-20-like Kinase 1/2 (MST1/2) Inhibitor XMU-MP-1 Improves Glucose Tolerance in Streptozotocin-Induced Diabetes Mice.Molecules (Basel, Switzerland) · 2020Article
- Common gut microbial metabolites of dietary flavonoids exert potent protective activities in β-cells and skeletal muscle cells.The Journal of nutritional biochemistry · 2018Article
- Enhanced Expression of the Key Mitosis Regulator Cyclin B1 Is Mediated by PDZ-Binding Kinase in Islets of Pregnant Mice.Journal of the Endocrine Society · 2018Article
- High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds.Journal of visualized experiments : JoVE · 2018Article
- Changes of MODY signal pathway genes in the endoplasmic reticulum stress in INS-1-3 cells.PloS one · 2018Article
- The Orphan Nuclear Receptor 4A1: A Potential New Therapeutic Target for Metabolic Diseases.Journal of diabetes research · 2018Review
- ARD1-mediated aurora kinase A acetylation promotes cell proliferation and migration.Oncotarget · 2017Article
- Advances in pancreatic islet monolayer culture on glass surfaces enable super-resolution microscopy and insights into beta cell ciliogenesis and proliferation.Scientific reports · 2017Article
- PAX4 promotes PDX1-induced differentiation of mesenchymal stem cells into insulin-secreting cells.American journal of translational research · 2017Article
- Cdk5r1 Overexpression Induces Primary β-Cell Proliferation.Journal of diabetes research · 2016Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 and type 2 diabetes are ultimately characterized by depleted β-cell mass. Characterization of the molecular pathways that control β-cell proliferation could be harnessed to restore these cells. The homeobox β-cell transcription factor Nkx6.1 induces β-cell proliferation by activating the orphan nuclear receptors Nr4a1 and Nr4a3. Here, we demonstrate that Nkx6.1 localizes to the promoter of the mitotic kinase AURKA (Aurora Kinase A) and induces its expression. Adenovirus mediated overexpression of AURKA is sufficient to induce proliferation in primary rat islets while maintaining glucose stimulated insulin secretion. Furthermore, AURKA is necessary for Nkx6.1 mediated β-cell proliferation as demonstrated by shRNA mediated knock down and pharmacological inhibition of AURKA kinase activity. AURKA preferentially induces DNA replication in β-cells as measured by BrdU incorporation, and enhances the rate of histone H3 phosphorylation in primary β-cells, demonstrating that AURKA induces the replicative and mitotic cell cycle phases in rat β-cells. Finally, overexpression of AURKA results in phosphorylation of the cell cycle regulator p53, which targets p53 for degradation and permits cell cycle progression. These studies define a pathway by which AURKA upregulation by Nkx6.1 results in phosphorylation and degradation of p53, thus removing a key inhibitory factor and permitting engagement of the β-cell proliferation pathway.
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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.