2.7.7.23	evolution	although Entamoeba histolytica UAP exhibits the same three-domain global architecture as other UAPs, it appears to lack three alpha-helices at the N-terminus and contains two amino acids in the allosteric pocket that make it appear more like the enzyme from the human host than that from the other parasite Trypanosoma brucei	737391	
2.7.7.23	evolution	comparison of the activities of the ST0452 protein to those of similar enzymes from bacteria show that both the apparent Km and kcat values of the ST0452 GlcNAc-1-P UTase activity are smaller than those of Escherichia coli GlmU (EcGlmU) enzymes indicating that the archaeal ST0452 protein can accept a low concentration of substrate but that its turnover rate is lower than that of the EcGlmU enzyme	-, 755852	
2.7.7.23	evolution	GlmU belongs to the large family of sugar nucleotidyl transferases, which can be classified into group-I, which employs the two-metal mechanism-B as in GlmU, and group-II that employs a variant one metal mechanism-B, wherein the role of Mg2+ A is substituted by a conserved lysine. Eukaryotic sugar nucleotidyl transferases appear confined to group-II, structure-based sequence comparisons of sugar nucleotidyl transferases	740866	
2.7.7.23	evolution	organization andexpression of the mmy gene in Drosophila species, overview	738089	
2.7.7.23	evolution	the GlmU proteins encoded by Yersinia pestis and Yersinia pseudotuberculosis are identical in amino acid sequence	-, 735569	
2.7.7.23	evolution	the N-acetylglucosamine-1-phosphate uridyltransferase (GlmU) is a bifunctional enzyme exclusive to prokaryotes, that belongs to the family of sugar nucleotidyltransferases (SNTs)	735396	
2.7.7.23	evolution	UAP isozymes are encoded by two different genes, LmUAP1 and LmUAP2	739475	
2.7.7.23	malfunction	GlmUMtb depletion perturbs cell wall structure and affects the bacterial survival in normoxia, overview	-, 737150	
2.7.7.23	malfunction	independently-derived mmy mutants exhibit a variety of highly penetrant phenotypes, ranging from cuticle defects associated with a failure to synthesize chitin to cuticle defects associated with well-characterized Dpp-dependent closure abnormalities (dorsal closure and head involution). In particular, the mmy-associated cuticle defects are identical to those resulting from loss-of-function mutations in raw and anterior-open	738089	
2.7.7.23	malfunction	knockdown of LdUAP1 reduces chitin contents in whole larvae and integument samples, thins tracheal taenidia, impairs larval-larval molt, larval-pupal ecdysis and adult emergence. Combined knockdown of LdUAP1 and LdUAP2 causes an additive negative effect. Phenotypes, overview	738383