Catalyzes the transfer of N-acetylglucosamine (GlcNAc) to core 2 branched O-glycans. Necessary for the synthesis of type III mucin which is specifically produced in the stomach, duodenum, and pancreatic duct. May protect against inflammation-associated gastric adenocarcinoma. Protein modification; protein glycosylation. The conserved DXD motif is involved in enzyme activity. Viable with no gross defects. Gastric mucosa cells and duodenal Brunner's glands have an altered O-linked glycosylation profile with complete loss of terminal alpha-1,4-linked N-acetylglucosamine residues (alpha-GlcNAc). Animals develop spontaneous gastric adenocarcinomas, with all individuals affected by 60 weeks of age. Hyperplasia of surface mucous cells and pyloric gland cells is observed as early as 5 weeks of age, associated with increased inflammatory responses in the gastric mucosa. Belongs to the glycosyltransferase 32 family.