1.5.1.33: pteridine reductase
This is an abbreviated version!
For detailed information about pteridine reductase, go to the full flat file.
Word Map on EC 1.5.1.33
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1.5.1.33
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leishmania
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dihydrofolate
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trypanosoma
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antileishmanial
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antifolate
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promastigotes
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leishmaniasis
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trypanosomatids
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pterins
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donovani
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amastigotes
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trypanosomiasis
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dhfr-t
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trypanothione
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reductase-thymidylate
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tarentolae
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dihydrobiopterin
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glucantime
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medicine
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drug development
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pharmacology
- 1.5.1.33
- leishmania
- dihydrofolate
- trypanosoma
-
antileishmanial
- antifolate
- promastigotes
- leishmaniasis
-
trypanosomatids
- pterins
- donovani
- amastigotes
- trypanosomiasis
-
dhfr-t
- trypanothione
-
reductase-thymidylate
- tarentolae
- dihydrobiopterin
-
glucantime
- medicine
- drug development
- pharmacology
Reaction
Synonyms
Atu1130, EC 1.1.1.253, H region methotrexate resistance protein, LaPTR1, LbPTR1, LdPTR1, LmPTR1, LpPTR1, More, NADPH-dependent short-chain dehydrogenase/reductase pteridine reductase, NADPH-dihydropteridine reductase, PruA, pteridine reductase, pteridine reductase 1, pteridine reductase I, PTR1, reductase, dihydropteridine (reduced nicotinamide adenine dinucleotide phosphate), Tb-PR, TbPTR1, tcptr1
ECTree
1.5.1.33 pteridine reductaseAdvanced search results
results (
results (Engineering
Engineering on EC 1.5.1.33 - pteridine reductase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
R24A
site-directed mutagenesis, reduced activity compared to wild-type
R24G
site-directed mutagenesis, highly reduced activity compared to wild-type
Y161A
site-directed mutagenesis, slightly reduced activity compared to wild-type
Y161F/Y163F
site-directed mutagenesis, reduced activity compared to wild-type
Y163F
site-directed mutagenesis, slightly reduced catalytic efficiency but increased activity compared to wild-type
R24A
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site-directed mutagenesis, reduced activity compared to wild-type
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Y161A
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site-directed mutagenesis, slightly reduced activity compared to wild-type
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Y163F
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site-directed mutagenesis, slightly reduced catalytic efficiency but increased activity compared to wild-type
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Y161A
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site-directed mutagenesis, slightly reduced activity compared to wild-type
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Y163F
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site-directed mutagenesis, slightly reduced catalytic efficiency but increased activity compared to wild-type
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K199E
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The mutant enzymes Y38D, Y195F, Y195W, and K199R are inactive even if they are purified as tetramers
Y175D
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mutant enzyme Y175D shows properties similar to wild type enzyme. The mutant enzymes Y38D, Y195F, Y195W, and K199R are inactive even if they are purified as tetramers
Y195F
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The mutant enzymes Y38D, Y195F, Y195W, and K199R are inactive even if they are purified as tetramers
Y195W
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The mutant enzymes Y38D, Y195F, Y195W, and K199R are inactive even if they are purified as tetramers
Y38D
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The mutant enzymes Y38D, Y195F, Y195W, and K199R are inactive even if they are purified as tetramers
additional information
additional information
mutational analysis of the PruA YX3K motif. Generation of an Agrobacterium. tumefaciens DELTApruA strain
additional information
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mutational analysis of the PruA YX3K motif. Generation of an Agrobacterium. tumefaciens DELTApruA strain
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additional information
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mutational analysis of the PruA YX3K motif. Generation of an Agrobacterium. tumefaciens DELTApruA strain
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additional information
a Leishmania infantum DHFR-TS null mutant is thymidine auxotroph showing a phenotype that can be rescued by the addition of thymidine or by transfection of the flavin-dependent bacterial thymidylate synthase (TS) gene ThyX. In DHFR-TS null mutants, it is impossible to obtain a chromosomal null mutant of PTR1 except if DHFR-TS or PTR1 are provided episomally. Episomal expression of PTR1 in these cells does not revert thymidine auxotrophy. Leishmania can survive without copies of either DHFR-TS or PTR1 but not without both. Provided that the results observed with the insect stage parasites are also replicated with intracellular parasites, it suggests that antifolate therapy in Leishmania only works if both DHFRTS and PTR1 are targeted simultaneously. Generation of a PTR1 null mutant in the DHFR-TSNEO/HYG cells using puromycin (PURO) and zeocin (ZEO) inactivation cassettes. Transfection of the PURO cassette in DHFR-TSNEO/HYG cloned cells leads to PTR1PURO/+ parasites. Transfection of the ZEO cassette in these parasites leads to the correct integration at the PTR1 locus but with a remaining intact copy of PTR1 in the population of cells analyzed. DHFR-TSNEO/HYG PTR1PURO/+ cells are complemented with episomally-expressed ThyX. These cells are able to grow in the absence of thymidine supplementation. Upon the transfection of the ZEO PTR1-inactivation cassette integration at the right locus is ontained but the hybridization signals are consistent with the population of parasites having the PTR1PURO/ZEO/+ genotype. This PTR1PURO/ZEO/+ genotype is also obtained in an independent PTR1 gene knockout experiment where ThyX is episomally expressed. When the genetic complementation is done with DHFR-TS instead of ThyX, the transfection of the ZEO PTR1-inactivation leads to a PTR1 chromosomal null mutant
additional information
-
a Leishmania infantum DHFR-TS null mutant is thymidine auxotroph showing a phenotype that can be rescued by the addition of thymidine or by transfection of the flavin-dependent bacterial thymidylate synthase (TS) gene ThyX. In DHFR-TS null mutants, it is impossible to obtain a chromosomal null mutant of PTR1 except if DHFR-TS or PTR1 are provided episomally. Episomal expression of PTR1 in these cells does not revert thymidine auxotrophy. Leishmania can survive without copies of either DHFR-TS or PTR1 but not without both. Provided that the results observed with the insect stage parasites are also replicated with intracellular parasites, it suggests that antifolate therapy in Leishmania only works if both DHFRTS and PTR1 are targeted simultaneously. Generation of a PTR1 null mutant in the DHFR-TSNEO/HYG cells using puromycin (PURO) and zeocin (ZEO) inactivation cassettes. Transfection of the PURO cassette in DHFR-TSNEO/HYG cloned cells leads to PTR1PURO/+ parasites. Transfection of the ZEO cassette in these parasites leads to the correct integration at the PTR1 locus but with a remaining intact copy of PTR1 in the population of cells analyzed. DHFR-TSNEO/HYG PTR1PURO/+ cells are complemented with episomally-expressed ThyX. These cells are able to grow in the absence of thymidine supplementation. Upon the transfection of the ZEO PTR1-inactivation cassette integration at the right locus is ontained but the hybridization signals are consistent with the population of parasites having the PTR1PURO/ZEO/+ genotype. This PTR1PURO/ZEO/+ genotype is also obtained in an independent PTR1 gene knockout experiment where ThyX is episomally expressed. When the genetic complementation is done with DHFR-TS instead of ThyX, the transfection of the ZEO PTR1-inactivation leads to a PTR1 chromosomal null mutant
additional information
-
a Leishmania infantum DHFR-TS null mutant is thymidine auxotroph showing a phenotype that can be rescued by the addition of thymidine or by transfection of the flavin-dependent bacterial thymidylate synthase (TS) gene ThyX. In DHFR-TS null mutants, it is impossible to obtain a chromosomal null mutant of PTR1 except if DHFR-TS or PTR1 are provided episomally. Episomal expression of PTR1 in these cells does not revert thymidine auxotrophy. Leishmania can survive without copies of either DHFR-TS or PTR1 but not without both. Provided that the results observed with the insect stage parasites are also replicated with intracellular parasites, it suggests that antifolate therapy in Leishmania only works if both DHFRTS and PTR1 are targeted simultaneously. Generation of a PTR1 null mutant in the DHFR-TSNEO/HYG cells using puromycin (PURO) and zeocin (ZEO) inactivation cassettes. Transfection of the PURO cassette in DHFR-TSNEO/HYG cloned cells leads to PTR1PURO/+ parasites. Transfection of the ZEO cassette in these parasites leads to the correct integration at the PTR1 locus but with a remaining intact copy of PTR1 in the population of cells analyzed. DHFR-TSNEO/HYG PTR1PURO/+ cells are complemented with episomally-expressed ThyX. These cells are able to grow in the absence of thymidine supplementation. Upon the transfection of the ZEO PTR1-inactivation cassette integration at the right locus is ontained but the hybridization signals are consistent with the population of parasites having the PTR1PURO/ZEO/+ genotype. This PTR1PURO/ZEO/+ genotype is also obtained in an independent PTR1 gene knockout experiment where ThyX is episomally expressed. When the genetic complementation is done with DHFR-TS instead of ThyX, the transfection of the ZEO PTR1-inactivation leads to a PTR1 chromosomal null mutant
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