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Loss of complex O-glycosylation impairs exocrine pancreatic function and induces MODY8-like diabetes in mice
oleh: Gerrit Wolters-Eisfeld, Baris Mercanoglu, Bianca T. Hofmann, Thomas Wolpers, Claudia Schnabel, Sönke Harder, Pascal Steffen, Kai Bachmann, Babett Steglich, Jörg Schrader, Nicola Gagliani, Hartmut Schlüter, Cenap Güngör, Jakob R. Izbicki, Christoph Wagener, Maximilian Bockhorn
Format: | Article |
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Diterbitkan: | Nature Publishing Group 2018-10-01 |
Deskripsi
Pancreatic disorders: when protein modification misfires Reduced levels of a protein called Cosmc in the pancreas may lead to pancreatic disorders and a rare form of diabetes. Disruption to glycosylation, the process by which carbohydrates are added to proteins, can have significant knock-on effects for cellular functioning. Gerrit Wolters-Eisfeld at the University Medical Center Hamburg-Eppendorf, Germany, and co-workers used mouse models to demonstrate the importance of correct formation of one type of carbohydrate, O-glycans, for normal pancreatic function. The team generated mice without Cosmc, a molecule that assists with O-glycosylation. Loss of Cosmc in the pancreas resulted in shortened O-glycans and pancreatic insufficiency. However, one protein called Cel was modified in abundance; this may be further bad news because mutations in Cel are linked to the onset of a rare form of diabetes.