EC Number   |
General Information |
Reference |
|---|
   5.4.99.9 | evolution |
all organisms that generate Galf-containing glycans encode a UGM homologue |
746590 |
| 5.4.99.9 | evolution |
conserved active site residues in Aspegillus fumigatus UGM compared to prokaryotic UGMs, overview |
727899 |
| 5.4.99.9 | evolution |
substrate recognition of bacterial and eukaryotic enzyme, involving a dynamic Arg, conserved steric interactions, and enzyme-substrate noncovalent interactions, overview. Domain 1 is important for positioning Galp for nucleophilic attack, domain 2 provides most of the interactions with the uridine group, and domain 3 figures prominently in binding the diphosphate |
-, 726820 |
| 5.4.99.9 | evolution |
substrate recognition of bacterial and eukaryotic enzyme, involving a dynamic Arg, conserved steric interactions, and enzyme-substrate noncovalent interactions, overview. Domain 1 is important for positioning Galp for nucleophilic attack, domain 2 provides most of the interactions with the uridine group, and domain 3 figures prominently in binding the pyrophosphate |
726820 |
| 5.4.99.9 | evolution |
the enzyme belongs to the group of flavoenzymes, a unifying concept of flavin hot spots is introduced to understand and categorize the mechanisms and reactivities of both traditional and noncanonical flavoenzymes. The major hot spots of reactivity include the N5, C4a, and C4O atoms of the isoalloxazine, and the 20 hydroxyl of the ribityl chain. The role of hot spots in traditional flavoenzymes, such as monooxygenases, and description of flavin hot spots in noncanonical flavoenzymes, overview |
746922 |
| 5.4.99.9 | evolution |
the enzyme is a member of the UGM family |
-, 727319 |
| 5.4.99.9 | malfunction |
AfUgmA residues R182 and R327 are important for its function in vivo, with even conservative amino (RK) substitutions producing AnugmADELTA-phenotype strains. Loss of cell wall alpha-D-galactofuranose is associated with increased hyphal surface adhesion. AfUgmA active site mutations do not affect UgmA-GFP cytoplasmic distribution. Mutant phenotypes, overview |
749145 |
| 5.4.99.9 | malfunction |
Aspergillus nidulans strains deleted for UgmA lack immunolocalizable UDP-D-galactofuranose, have growth and sporulation defects, abnormal wall architecture, and significantly larger hyphal surface subunits and lower cell wall viscoelastic moduli |
714878 |
| 5.4.99.9 | malfunction |
deletion or repression of Aspergillus nidulans gene ugmA (AnugmA), involved in galactofuranose biosynthesis, impairs growth and increases sensitivity to caspofungin, a beta-1,3-glucan synthesis antagonist. Alteration in galactofuranose affects wall glucan composition in Aspergillus nidulans. Wild-type and complemented wild-type hyphal walls have relatively low alpha-glucan content compared to mutant and AnugmADELTA strains. Mutant phenotypes, overview |
-, 749145 |
| 5.4.99.9 | malfunction |
glf-1 mutants display significant late embryonic and larval lethality, and other phenotypes indicative of defective surface coat synthesis, the glycan-rich outermost layer of the nematode cuticle |
-, 703365 |
