EC Number   |
General Information |
Reference |
|---|
   1.5.1.33 | evolution |
PTR1 is a NADPH-dependent enzyme belonging to the short-chain dehydrogenase/reductase (SDR) family |
765513 |
| 1.5.1.33 | evolution |
PTR1 is a short-chain dehydrogenase reductase family member. The trypanosomatid PTR1s are structurally very similar, sequence comparisons |
765417 |
| 1.5.1.33 | evolution |
PTR2 is a short-chain dehydrogenase reductase family member. In Trypanosoma cruzi, TcPTR1 and TcPTR2 are isoforms that show very high sequence homology but also display varied enzymatic activity. TcPTR1 in comparison to TcPTR2 shows higher activity with biopterin and folate than with H2F or H2B |
765417 |
| 1.5.1.33 | evolution |
the enzyme belong to the short-chain dehydrogenase/reductase (SDR) family of enzymes. Despite the overall low sequence identity among members of the SDR family (about 15-30%), a central catalytic YX3K motif is highly conserved, as is an N-terminal glycine motif (TGX3GXG), involved in cofactor binding and recognition. The pteridine reductases in the SDR family have an arginine in place of the glycine at position 6 in this motif (TGX3RXG) |
-, 765008 |
| 1.5.1.33 | malfunction |
comparisons of isogenic lines shows that ptr1-null mutants are 18fold more sensitive to H2O2 than PTR1-overproducing lines, and significant 3-5fold differences are seen with a broad panel of oxidant-inducing agents |
711796 |
| 1.5.1.33 | malfunction |
impossible to generate PTR1 null mutants. RNA interference results in complete knockdown of endogenous protein after 48 h, followed by cell death after 4 days. Lethal phenotype is reversed by expression of PTR1 in RNAi lines or by addition of tetrahydrobiopterin to cultures. Loss of PTR1 is associated with gross morphological changes due to a defect in cytokinesis, resulting in cells with multiple nuclei and kinetoplasts, as well as multiple detached flagella. Electron microscopy also reveal increased numbers of glycosomes, while immunofluorescence microscopy show increased and more diffuse staining for glycosomal matrix enzymes, indicative of mis-localisation to the cytosol. RNAi cell lines are markedly less virulent than wild-type parasites in mice |
713060 |
| 1.5.1.33 | malfunction |
Leishmania can survive without copies of either DHFR-TS or PTR1 but not without both. Leishmania is pterin auxotroph but a PTR1 knockout cell will grow well if sufficient reduced pterins are available |
-, 765644 |
| 1.5.1.33 | malfunction |
the mutant DELTApruA strain exhibits elevated biofilm formation and abundant polysaccharide production independent of surface contact. The plasmid-borne expression of wild-type PruA fully corrects this deficiency, while a plasmid-encoded PruA Y163A mutant variant expressed in the DELTApruA strain has no effect on these DELTApruA mutant phenotypes, with its phenotype appearing similar to the phenotype of the deletion strain alone |
-, 765008 |
| 1.5.1.33 | metabolism |
folates are reduced in Leishmania by the bifunctional dihydrofolate reductase thymidylate synthase (DHFR-TS) and by pteridine reductase (PTR1) |
-, 765644 |
| 1.5.1.33 | metabolism |
key enzymes involved in trypanosome folate metabolism are dihydrofolate reductase (DHFR) and pteridine reductase (PTR1) |
765417 |
