EC Number |
General Information |
Reference |
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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 |