ArticleDiabetologia2016
RNA-binding protein CUGBP1 regulates insulin secretion via activation of phosphodiesterase 3B in mice.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Curriculum vitae of CUG binding protein 1 (CELF1) in homeostasis and diseases: a systematic review.Cellular & molecular biology letters · 2024Pooled it
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- Adipocyte RNA-binding protein CELF1 promotes beiging of white fat through stabilizing Dio2 mRNA.Nature communications · 2025Article
- Orchestrating Nutrient Homeostasis: RNA-Binding Proteins as Molecular Conductors in Metabolic Disease Pathogenesis.Nutrients · 2025Review
- PARN Maintains RNA Stability to Regulate Insulin Maturation and GSIS in Pancreatic β Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- circGlis3 promotes β-cell dysfunction by binding to heterogeneous nuclear ribonucleoprotein F and encoding Glis3-348aa protein.iScience · 2024Article
- Rab26 restricts insulin secretion via sequestering Synaptotagmin-1.PLoS biology · 2023Article
- Article
- Advances in the study of RNA-binding proteins in diabetic complications.Molecular metabolism · 2022Review
- CUGBP1, a crucial factor for heart regeneration in mice.Cell death & disease · 2022Article
- Posttranscriptional Regulation of Insulin Resistance: Implications for Metabolic Diseases.Biomolecules · 2022Review
- Post-transcriptional control by RNA-binding proteins in diabetes and its related complications.Frontiers in physiology · 2022Review
- Targeting QKI-7 in vivo restores endothelial cell function in diabetes.Nature communications · 2020Article
- Stress-Induced Translational Regulation Mediated by RNA Binding Proteins: Key Links to β-Cell Failure in Diabetes.Diabetes · 2020Review
- mRNA Processing: An Emerging Frontier in the Regulation of Pancreatic β Cell Function.Frontiers in genetics · 2020Review
- Long Noncoding RNAs and RNA-Binding Proteins in Oxidative Stress, Cellular Senescence, and Age-Related Diseases.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisCUG-binding protein 1 (CUGBP1) is a multifunctional RNA-binding protein that regulates RNA processing at several stages including translation, deadenylation and alternative splicing, as well as RNA stability. Recent studies indicate that CUGBP1 may play a role in metabolic disorders. Our objective was to examine its role in endocrine pancreas function through gain- and loss-of-function experiments and to further decipher the underlying molecular mechanisms.
methodsA mouse model in which type 2 diabetes was induced by a high-fat diet (HFD; 60% energy from fat) and mice on a standard chow diet (10% energy from fat) were compared. Pancreas-specific CUGBP1 overexpression and knockdown mice were generated. Different lengths of the phosphodiesterase subtype 3B (PDE3B) 3' untranslated region (UTR) were cloned for luciferase reporter analysis. Purified CUGBP1 protein was used for gel shift experiments.
resultsCUGBP1 is present in rodent islets and in beta cell lines; it is overexpressed in the islets of diabetic mice. Compared with control mice, the plasma insulin level after a glucose load was significantly lower and glucose clearance was greatly delayed in mice with pancreas-specific CUGBP1 overexpression; the opposite results were obtained upon pancreas-specific CUGBP1 knockdown. Glucose- and glucagon-like peptide1 (GLP-1)-stimulated insulin secretion was significantly attenuated in mouse islets upon CUGBP1 overexpression. This was associated with a strong decrease in intracellular cAMP levels, pointing to a potential role for cAMP PDEs. CUGBP1 overexpression had no effect on the mRNA levels of PDE1A, 1C, 2A, 3A, 4A, 4B, 4D, 7A and 8B subtypes, but resulted in increased PDE3B expression. CUGBP1 was found to directly bind to a specific ATTTGTT sequence residing in the 3' UTR of PDE3B and stabilised PDE3B mRNA. In the presence of the PDE3 inhibitor cilostamide, glucose- and GLP-1-stimulated insulin secretion was no longer reduced by CUGBP1 overexpression. Similar to CUGBP1, PDE3B was overexpressed in the islets of diabetic mice. CONCLUSIONS/
interpretationWe conclude that CUGBP1 is a critical regulator of insulin secretion via activating PDE3B. Repressing this protein might provide a potential strategy for treating type 2 diabetes.
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