EC Number   |
General Information |
Reference |
|---|
    3.5.2.9 | evolution |
comparative analysis of prokaryotic genomes shows that the gene encoding pyroglutamyl peptidase, which removes N-terminal 5-oxoproline residues, clusters in diverse genomes with genes specifying homologs of a fungal lactamase (renamed prokaryotic 5-oxoprolinase A, pxpA) and homologs of allophanate hydrolase subunits (renamed pxpB and pxpC). 5-Oxoproline is a major universal metabolite damage product and its disposal systems are common in all domains of life |
-, 757181 |
| 3.5.2.9 | evolution |
detailed phylogenetic analysis of 5-oxoprolinases, overview |
-, 756535 |
| 3.5.2.9 | evolution |
phylogenetic analysis suggests a relationship between taxonomic grouping and PxpA oligomerization |
-, 756017 |
| 3.5.2.9 | malfunction |
5-oxo-L-proline is a competitive inhibitor for glutamate transport in Sulfolobus solfataricus. The growth inhibiting effect of 5-oxo-L-proline on the cell culture is not only due to the loss of available carbon, because its addition to a growing culture can lead to cell death |
-, 755916 |
| 3.5.2.9 | malfunction |
deletion of FgOXP1 or FgOXP2 in Fusarium graminearum leads to significant defects in its virulence on wheat, likely caused by an observed decreased deoxynivalenol (DON, a mycotoxin) production in the gene deletion mutant strains. DON is one of the best characterized virulence factors of Fusarium graminearum. The FgOXP2 deletion mutant strains are also defective in conidiation and sexual reproduction while the FgOXP1 deletion mutant strains are normal for those phenotypes. Double deletion of FgOXP1 and FgOXP2 leads to more severe defects in conidiation, DON production and virulence on plants, suggesting that both FgOXP1 and FgOXP2 play a role in fungal development and plant colonization. Although transformation of the enzyme from Magnaporthe oryzae wild-type strain 70-15, MoOXP1, into DELTAFgoxp1 is able to complement DELTAFgoxp1, transformation of MoOXP1 into DELTAFgoxp2 fails to restore its defects in sexual development, DON production, and pathogenicity. Defects noticed in the gene deletion mutant strains of 5-oxoprolinase in Fusarium graminearum are caused by the affected gamma-glutamyl cycle, phenotypes, overview |
-, 756535 |
| 3.5.2.9 | malfunction |
deletion of FgOXP1 or FgOXP2 in Fusarium graminearum leads to significant defects in its virulence on wheat, likely caused by an observed decreased deoxynivalenol (DON, a mycotoxin) production in the gene deletion mutant strains. DON is one of the best characterized virulence factors of Fusarium graminearum. The FgOXP2 deletion mutant strains are also defective in conidiation and sexual reproduction while the FgOXP1 deletion mutant strains are normal for those phenotypes. Double deletion of FgOXP1 and FgOXP2 leads to more severe defects in conidiation, DON production and virulence on plants, suggesting that both FgOXP1 and FgOXP2 play a role in fungal development and plant colonization. Although transformation of the enzyme from Magnaporthe oryzae wild-type strain 70-15, MoOXP1, into DELTAFgoxp1, transformation of MoOXP1 into DELTAFgoxp2 fails to restore its defects in sexual development, DON production, and pathogenicity. Defects noticed in the gene deletion mutant strains of 5-oxoprolinase in Fusarium graminearum are caused by the affected gamma-glutamyl cycle, phenotypes, overview |
-, 756535 |
| 3.5.2.9 | malfunction |
inactivation of Bacillus subtilis pxpA, pxpB, or pxpC genes slows growth, causes 5-oxoproline accumulation in cells and medium, and prevents use of 5-oxoproline as a nitrogen source. ATP-dependent 5-oxoprolinase activity disappears when pxpA, pxpB, or pxpC is inactivated |
-, 757181 |
| 3.5.2.9 | malfunction |
inherited 5-oxoprolinase deficiency is a rare 5-oxoprolinase deficiency is an extremely rare disorder of the gamma-glutamyl cycle characterised by 5-oxoprolinuria, heterogeneity of the clinical presentation which ranges from normal to significant neurological involvement, genotype-phenotype correlation, phenotypes, overview |
733676 |
| 3.5.2.9 | malfunction |
inherited 5-oxoprolinase deficiency is a rare inborn condition characterised by 5-oxoprolinuria. Three enzyme mutations are involved: p.H870Pfs in a homozygous state, which results in a truncated protein, and two heterozygous missense changes, S323R and V1089I |
733792 |
| 3.5.2.9 | metabolism |
comparison of the effect of 5-oxoproline on the growth of Sulfolobus solfataricus and the closely related crenarchaeon Sulfolobus acidocaldarius. Sulfolobus solfataricus shows intracellular accumulation of 5-oxoproline and crude cell extract assays show a less effective degradation of 5-oxoproline. Sulfolobus acidocaldarius seems to be less versatile regarding carbohydrates and prefers peptidolytic growth compared to Sulfolobus solfataricus. Concludingly, Sulfolobus acidocaldarius exhibits a more efficient utilization of 5-oxoproline and is not inhibited by this compound, making it a better candidate for applications with glutamate-containing media at high temperatures |
-, 755916 |
