ArticleInternational journal of molecular medicine2017
Phosphorylation of carboxypeptidase B1 protein regulates β-cell proliferation.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- Carboxypeptidase B1 in dialyzed chronic kidney disease patients.Scientific reports · 2025Article
- Proteomic and Bioinformatic Analysis of Decellularized Pancreatic Extracellular Matrices.Molecules (Basel, Switzerland) · 2021Article
- Short Duration Alagebrium Chloride Therapy Prediabetes Does Not Inhibit Progression to Autoimmune Diabetes in an Experimental Model.Metabolites · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A reduction in pancreatic islet β-cells leads to the onset of diabetes. Hence, the identification of the mechanisms inducing β-cell proliferation is important for developing a treatment course against the disease. It has been well established that post-translational modifications (PTMs) of proteins affect their functionality. In addition, PTMs have been suggested to play important roles in organ regeneration. Therefore, in this study, we investigated PTMs associated with pancreatic regeneration using two-dimensional electrophoresis. Four carboxypeptidase B1 (CPB1) proteins were identified at different isoelectric points, with the same molecular weight. The motif of CPB1 PTMs was identified by mass spectrophotometry, and the downregulation of CPB1 phosphorylation in pancreatectomy was confirmed. The dephosphorylation of CPB1 induced β-cell proliferation. We thus surmise that the altered PTM of CPB1 is associated with pancreatic regeneration.
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