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Phosphorylation of carboxypeptidase B1 protein regulates β-cell proliferation

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...

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Detalles Bibliográficos
Autores principales: Yu, Seong-Lan, Han, Seungyun, Kim, Hong Rye, Park, Jong Woo, Jin, Dong Il, Kang, Jaeku
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5627887/
https://www.ncbi.nlm.nih.gov/pubmed/28949379
http://dx.doi.org/10.3892/ijmm.2017.3141
Descripción
Sumario: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.