ArticleEMBO molecular medicine2021
Menin-regulated Pbk controls high fat diet-induced compensatory beta cell proliferation.
Article in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Inhibiting menin attenuates high-fat diet-induced weight gain by limiting intestinal lipid absorption in mice.The Journal of clinical investigation · 2026Article
- Elevated Plasma T-LAK cell-originated protein kinase Owned the Potential for Predicting Favorable Outcomes in Acute Ischemic Stroke Patients.Cellular and molecular neurobiology · 2026Article
- T‑cadherin and its impact on human diseases (Review).Molecular medicine reports · 2026Review
- HDAC3-driven immunometabolic reprogramming in type 2 diabetes and its complications: from enzymatic deacetylation to non-enzymatic scaffolding.Frontiers in immunology · 2026Review
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- The Impact of BMI on PCOS Patients and Transcriptome Profiling and Bioinformatic Analysis of Granulosa Cells in PCOS Patients with High and Low BMI.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- New Molecules in Type 2 Diabetes: Advancements, Challenges and Future Directions.International journal of molecular sciences · 2024Review
- Role of transcription factor FOXM1 in diabetes and its complications (Review).International journal of molecular medicine · 2023Article
- Restored UBE2C expression in islets promotes β-cell regeneration in mice by ubiquitinating PER1.Cellular and molecular life sciences : CMLS · 2023Article
- Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling.iScience · 2022Article
- Menin-regulated Pbk controls high fat diet-induced compensatory beta cell proliferation.EMBO molecular medicine · 2021Article
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic beta cells undergo compensatory proliferation in the early phase of type 2 diabetes. While pathways such as FoxM1 are involved in regulating compensatory beta cell proliferation, given the lack of therapeutics effectively targeting beta cell proliferation, other targetable pathways need to be identified. Herein, we show that Pbk, a serine/threonine protein kinase, is essential for high fat diet (HFD)-induced beta cell proliferation in vivo using a Pbk kinase deficiency knock-in mouse model. Mechanistically, JunD recruits menin and HDAC3 complex to the Pbk promoter to reduce histone H3 acetylation, leading to epigenetic repression of Pbk expression. Moreover, menin inhibitor (MI) disrupts the menin-JunD interaction and augments Pbk transcription. Importantly, MI administration increases beta cell proliferation, ameliorating hyperglycemia, and impaired glucose tolerance (IGT) in HFD-induced diabetic mice. Notably, Pbk is required for the MI-induced beta cell proliferation and improvement of IGT. Together, these results demonstrate the repressive role of the menin/JunD/Pbk axis in regulating HFD-induced compensatory beta cell proliferation and pharmacologically regulating this axis may serve as a novel strategy for type 2 diabetes therapy.
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