2.4.1.144	additional information	-	
2.4.1.144	additional information	the biantennary structure of a core mannose is twisted in presence of bisecting GlcNAc, probably responsible for the substrate inaccessibility to N-acetylglucosamine transferase V to form the beta-1,6 structure	
2.4.1.144	additional information	in brain cells with down-regulated enzyme activity, normal prion proteins PrPC get conversed to pathogenic prion protein PrPSc due to a lower amount of glycans with bisecting N-acetylglucosamine residues	
2.4.1.144	additional information	biosynthetic pathway of the core structures of Asn-linked sugar chains, overview	
2.4.1.144	additional information	key enzyme that inhibits the extension of N-glycans by introducing a bisecting N-acetylglucosamine residue, modification of N-glycans by the enzyme affects a number of intracellular signalling pathways	
2.4.1.144	additional information	beta1,4-N-acetylglucosaminyltransferase III potentiates beta1 integrin-mediated neuritogenesis induced by serum deprivation in Neuro2a cells	
2.4.1.144	additional information	cell-cell interaction-dependent regulation of N-acetylglucosaminyltransferase III and the bisected N-glycans in GE11 epithelial cells	
2.4.1.144	additional information	N-acetylglucosaminyltransferase III expression is regulated by cell-cell adhesion via the E-cadherin-catenin-actin complex	
2.4.1.144	additional information	N-acetylglucosaminyltransferase III is a glycosyltransferase which produces bisected N-glycans by transferring GlcNAc to the 4-position of core mannose	
2.4.1.144	additional information	the MCAM glycoprotein, which is a biomarker of cutaneous melanoma, as a potential target for overexpressed glycosyltransferases