Loss of complex O-glycosylation impairs exocrine pancreatic function and induces MODY8-like diabetes in mice

@inproceedings{WoltersEisfeld2018LossOC,
  title={Loss of complex O-glycosylation impairs exocrine pancreatic function and induces MODY8-like diabetes in mice},
  author={Gerrit Wolters-Eisfeld and Baris Mercanoglu and Bianca T. Hofmann and Thomas Wolpers and Claudia Schnabel and S{\"o}nke Harder and Pascal Steffen and Kai A. Bachmann and Babett Steglich and Joerg Schrader and Nicola Gagliani and Hartmut Schl{\"u}ter and Cenap G{\"u}ng{\"o}r and Jakob Robert Izbicki and Christoph Wagener and Maximilian Bockhorn},
  booktitle={Experimental & Molecular Medicine},
  year={2018}
}
Cosmc is ubiquitously expressed and acts as a specific molecular chaperone assisting the folding and stability of core 1 synthase. Thus, it plays a crucial role in the biosynthesis of O-linked glycosylation of proteins. Here, we show that ablation of Cosmc in the exocrine pancreas of mice causes expression of truncated O-glycans (Tn antigen), resulting in exocrine pancreatic insufficiency with decreased activities of digestive enzymes and diabetes. To understand the molecular causes of the… CONTINUE READING
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