EC Number   |
General Information |
Reference |
|---|
    1.17.1.4 | evolution |
the enzyme belongs to the xanthine oxidase family |
745069 |
| 1.17.1.4 | evolution |
XDHs are widely distributed in all eukarya, bacteria and archaea domains, phylogenetic analysis |
-, 744450 |
| 1.17.1.4 | evolution |
XDHs are widely distributed in all eukarya, bacteria and archaea domains, phylogenetic analysis. The page XDH sequence shows 100% identity to the genomic XDH genes of Acinetobacter baumannii. It seems plausible that the similarity is a result of horizontal gene transfer |
744450 |
| 1.17.1.4 | evolution |
XDHs are widely distributed in all eukarya, bacteria and archaea domains, phylogenetic analysis. The unique industrially applicable Acinetobacter baumannii XDH shows only modest similarity to all the previous already-characterized XDHs |
744450 |
| 1.17.1.4 | malfunction |
disruption of XDH by allopurinol or XDH1 by RNA interference significantly affect mosquito survival, causing a disruption in blood digestion, excretion, oviposition, and reproduction. XDH1-deficient mosquitoes show a persistence of serine proteases in the midgut at 48 h after blood feeding and a reduction in the uptake of vitellogenin by the ovaries. Analysis of the fat body from dsRNA-XDH1-injected mosquitoes fall into 2 groups: one group is characterized by a reduction of the XDH1 transcript, whereas the other group is characterized by an upregulation of several transcripts, including XDH1, glutamine synthetase, alanine aminotransferase, catalase, superoxide dismutase, ornithine decarboxylase, glutamate receptor, and ammonia transporter. Depletion of XDH1 activity is lethal to bloodfed mosquitoes. Silencing of XDH1 reduces protein expression and delays synthesis and excretion of nitrogen waste, XDH1 deficiency slows digestion, vitellogenesis, and oviposition, and reduces fecundity |
744865 |
| 1.17.1.4 | malfunction |
dysfunction of purine degradation is a result of knocking down the key enzyme xanthine dehydrogenase, leading to severely reduced survival of Arabidopsis thaliana under progressive drought conditions and to significantly decreased tolerance to superoxide-mediated oxidative stress. The enhanced stress sensitivity of the knockdown mutants likely results from defective stress responses, because the drought-induced accumulation of the cellular protectant proline is compromised in the knockdown plants, which also show lower mRNA levels of P5CS1, the gene encoding the rate-limiting enzyme for proline biosynthesis, DELTA1-pyrroline-5-carboxylate synthase 1 |
-, 746009 |
| 1.17.1.4 | malfunction |
potassium oxonate-induced hyperuricemia can be reduced by oral application of onions reducing serum uric acid levels in hyperuricemic rats. The compound probably does not act via simple enzyme inhibition mechanism |
706057 |
| 1.17.1.4 | malfunction |
RNAi silencing of XDH1 in ecotype Col-0 results in autofluorescent object formation and infiltration of allopurinol, an inhibitor of XDH. drf1 Mutants contain missense mutations in XDH1, whole-cell and haustorial complex-confined H2O2 is significantly reduced in the mutants compared with the parental line |
-, 746031 |
| 1.17.1.4 | malfunction |
the powdery mildew fungus Golovinomyces cichoracearum triggers defense responses in Arabidopsis mediated by the R gene RPW8.2. In a screen for mutants defective in RPW8.2-related resistance to powdery mildew, three plants with point mutations in xanthine dehydrogenase 1 (XDH1), including two that alter residues strictly conserved among xanthine dehydrogenases. The mutants show impaired resistance to powdery mildew and accumulate less H2O2 in the haustorial complex in epidermal cells invaded by the fungus. These point mutations decrease the activity of recombinant XDH1 proteins, in terms of both dehydrogenase activity and ROS production. Xanthine accumulation in the mutants is further induced by pathogen inoculation due to increased purine catabolism (mediated at least in part by XDH1) upon infection. Feeding uric acid suppressed the H2O2 accumulation normally observed in mesophyll cells of infected xdh1 mutant plants |
-, 746030 |
| 1.17.1.4 | malfunction |
the retinoic acid deficiency in breast tumour epithelial cells has been ascribed to an insufficient expression of either the enzyme(s) involved in its biosynthesis or the cellular retinol binding protein or both, overview |
704789 |
