ArticlePloS one2014
C-Abl inhibitor imatinib enhances insulin production by β cells: c-Abl negatively regulates insulin production via interfering with the expression of NKx2.2 and GLUT-2.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Prunetin Attenuates Dexamethasone-Induced Pancreatic β-Cell Apoptosis: Modulation of Oxidative Stress and MAPK Signaling but Not Phosphorylated C-Abl Levels.Cell biochemistry and function · 2026Article
- Impact of Imatinib Therapy on Immunometabolism to Promote β-Cell Survival in Diabetes.Journal of diabetes · 2026Article
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Naphthoquinones mediate differentiation of human umbilical cord derived mesenchymal stem cells into insulin producing cells through regulation of Wnt and BMP pathways.BioImpacts : BI · 2026Article
- Exploration of Imatinib involved in amyloidogenesis as a common foundation for type-2 diabetes mellitus (T2DM) and Alzheimer's disease (AD).Metabolic brain disease · 2025Article
- The protective effect of imatinib against pancreatic β-cell apoptosis induced by dexamethasone via increased GSTP1 expression and reduced oxidative stress.Scientific reports · 2024Article
- The Role of Imatinib in Pediatric Type 1 Diabetes.JCEM case reports · 2024Article
- Future treatment of Diabetes - Tyrosine Kinase inhibitors.Journal of diabetes and metabolic disorders · 2023Review
- Are off-target effects of imatinib the key to improving beta-cell function in diabetes?Upsala journal of medical sciences · 2022Review
- Synergistic Effects of Milk-Derived Exosomes and Galactose onInternational journal of molecular sciences · 2021Review
- Beta Cell Therapies for Preventing Type 1 Diabetes: From Bench to Bedside.Biomolecules · 2020Review
- B lymphocytes protect islet β cells in diabetes prone NOD mice treated with imatinib.JCI insight · 2019Article
- Effect of imatinib on plasma glucose concentration in subjects with chronic myeloid leukemia and gastrointestinal stromal tumor.BMC endocrine disorders · 2018Article
- Immune Mechanisms and Pathways Targeted in Type 1 Diabetes.Current diabetes reports · 2018Review
- BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?TH open : companion journal to thrombosis and haemostasis · 2018Review
- c-Abl inhibition mitigates diet-induced obesity through improving insulin sensitivity of subcutaneous fat in mice.Diabetologia · 2017Article
- Novel members of quinoline compound family enhance insulin secretion in RIN-5AH beta cells and in rat pancreatic islet microtissue.Scientific reports · 2017Article
- An inhibitor of fibroblast growth factor receptor-1 (FGFR1) promotes late-stage terminal differentiation from NGN3+ pancreatic endocrine progenitors.Scientific reports · 2016Article
- Tyrosine Kinase Targeting: A Potential Therapeutic Strategy for Diabetes.Saudi journal of medicine & medical sciencesReview
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myelogenous leukemia patients treated with tyrosine kinase inhibitor, Imatinib, were shown to have increased serum levels of C-peptide. Imatinib specifically inhibits the tyrosine kinase, c-Abl. However, the mechanism of how Imatinib treatment can lead to increased insulin level is unclear. Specifically, there is little investigation into whether Imatinib directly affects β cells to promote insulin production. In this study, we showed that Imatinib significantly induced insulin expression in both glucose-stimulated and resting β cells. In line with this finding, c-Abl knockdown by siRNA and overexpression of c-Abl markedly enhanced and inhibited insulin expression in β cells, respectively. Unexpectedly, high concentrations of glucose significantly induced c-Abl expression, suggesting c-Abl may play a role in balancing insulin production during glucose stimulation. Further studies demonstrated that c-Abl inhibition did not affect the major insulin gene transcription factor, pancreatic and duodenal homeobox-1 (PDX-1) expression. Of interest, inhibition of c-Abl enhanced NKx2.2 and overexpression of c-Abl in β cells markedly down-regulated NKx2.2, which is a positive regulator for insulin gene expression. Additionally, we found that c-Abl inhibition significantly enhanced the expression of glucose transporter GLUT2 on β cells. Our study demonstrates a previously unrecognized mechanism that controls insulin expression through c-Abl-regulated NKx2.2 and GLUT2. Therapeutic targeting β cell c-Abl could be employed in the treatment of diabetes or β cell tumor, insulinoma.
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