This study investigates the impact of GalNT2 overexpression on pancreatic development and function. Conditional overexpression of GalNT2 in the pancreas causes acinar cell loss, pancreatic steatosis, and in homozygous mice, complete pancreatic loss and lethality. Proteomic analyses identified new O-glycosylation targets and support a role for GalNT2 in cellular transdifferentiation.
GalNT2 overexpression in the pancreas leads to loss of acinar cells, pancreatic steatosis, lethality in homozygous mice, and transdifferentiation into adipocytes. Proteomic analysis revealed additional O-glycosylation targets contributing to these phenotypes.
Conditional Galnt2 overexpression mouse model developed by genOway, with the Galnt2 transgene inserted into the Rosa26 locus. The model features a floxed STOP cassette allowing Cre-dependent overexpression, and was crossed with Ptf1a-Cre for pancreas-specific activation.
Pancreas development, O-glycosylation, Metabolic dysfunction, Cell fate reprogramming, Glycobiology
Conditional overexpression model, Rosa26 locus targeting, Floxed STOP cassette, Ptf1a-Cre driver, Tissue-specific activation, O-glycoproteomics
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
