Plays an essential role in protein N-glycosylation. Catalyzes the transfer of N-acetylglucosamine (GlcNAc) onto the free terminal mannose moiety in the core structure of the nascent N-linked glycan chain, giving rise to the second branch in complex glycans. N(4)-{beta-D-GlcNAc-(1->2)-alpha-D-Man-(1->3)-[alpha-D-Man-(1->6)]-beta-D-Man-(1->4)-beta-D-GlcNAc-(1->4)-beta-D-GlcNAc}-L-asparaginyl-[protein] + UDP-N-acetyl-alpha-D-glucosamine = H(+) + N(4)-{beta-D-GlcNAc-(1->2)-alpha-D-Man-(1->3)-[beta-D-GlcNAc-(1->2)-alpha-D-Man-(1->6)]-beta-D-Man-(1->4)-beta-D-GlcNAc-(1->4)-beta-D-GlcNAc}-L-asparaginyl-[protein] + UDP Protein modification; protein glycosylation. Homodimer. Detected in liver, lung, testis, kidney, brain, spleen, thymus, uterus and intestine. Decreased embryonic survival between 9 and 15 dpc. Surviving embryos are about 20% smaller than their littermates by 15 dpc. Most of the newborn pups die during the first week after birth, and none live longer than 4 weeks. Pups are about half the size of their littermates 8 days after birth, have dismorphic facial features and severe locomotor deficits. Pups display impaired muscle development and defects in bone development including a hunched spinal column, plus poorly calcified and brittle bones in vertebrae, ribs, femur and skull. Mutant mice have also mild anemia and impaired mucus production in the gastrointestinal system. Outcrossing increases the length of the lifespan, but does not increase the number of pups that survive after the fist week. Surviving males display testicular atrophy and are infertile. About one third of the surviving females produce offspring, but do not nurture their pups. Belongs to the glycosyltransferase 16 (GT16) protein family.