1.5.1.15: methylenetetrahydrofolate dehydrogenase (NAD+)
This is an abbreviated version!
For detailed information about methylenetetrahydrofolate dehydrogenase (NAD+), go to the full flat file.
Word Map on EC 1.5.1.15
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1.5.1.15
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homocysteine
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women
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case-control
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hyperhomocysteinemia
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leiden
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thrombosis
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artery
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folic
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prothrombin
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meta-analysis
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cardiovascular
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pregnancy
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thrombophilias
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venous
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children
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homozygote
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ethnic
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stroke
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coronary
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caucasian
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pcr-rflp
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smoking
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homozygosity
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thromboembolism
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one-carbon
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prothrombotic
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methotrexate
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thymidylate
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anticoagulant
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pubmed
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thermolabile
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embase
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hypercoagulable
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pai-1
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remethylation
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5-methyltetrahydrofolate
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gene-gene
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antithrombin
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pharmacogenetic
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cystathionine
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beta-synthase
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antiphospholipid
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reaction-restriction
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miscarriage
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medicine
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fxiii
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hypofibrinolysis
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homocystinuria
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anticardiolipin
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folate-dependent
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hinfi
- 1.5.1.15
- homocysteine
- women
-
case-control
- hyperhomocysteinemia
- leiden
- thrombosis
- artery
-
folic
- prothrombin
-
meta-analysis
- cardiovascular
- pregnancy
- thrombophilias
- venous
- children
-
homozygote
-
ethnic
- stroke
- coronary
-
caucasian
-
pcr-rflp
-
smoking
-
homozygosity
- thromboembolism
-
one-carbon
-
prothrombotic
- methotrexate
- thymidylate
-
anticoagulant
-
pubmed
-
thermolabile
-
embase
-
hypercoagulable
- pai-1
-
remethylation
- 5-methyltetrahydrofolate
-
gene-gene
- antithrombin
-
pharmacogenetic
- cystathionine
- beta-synthase
-
antiphospholipid
-
reaction-restriction
- miscarriage
- medicine
-
fxiii
-
hypofibrinolysis
- homocystinuria
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anticardiolipin
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folate-dependent
- hinfi
Reaction
Synonyms
5,10-CH2-THF dehydrogenase, 5,10-methylenetetrahydrofolate reductase, bifunctional N5,N10-methylene-H4F dehydrogenase/N5,N10-methenyltetrahydrofolate cyclohydrolase, FolD, methenyltetrahydrofolate cyclohydrolase, methylenetetrahydrofolate dehydrogenase (NAD+-dependent), methylenetetrahydrofolate dehydrogenase-cyclohydrolase, methylenetetrahydrofolate dehydrogenase-methenyltetrahydrofolate cyclohydrolase, methylenetetrahydrofolate dehydrogenase/cyclohydrolase, methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase, methylenetetrahydrofolate reductase, methyleneTHF dehydrogenase, Mg2+-/phosphate-dependent dehydrogenase, Mg2+/NAD-dependent methylenetetrahydrofolate dehydrogenase, More, MSMEG_6596, MSMEG_6649, MTD, MTHFD2, MTHFD2L, MTHFR, MTHFR1, MTHFR2, NAD+-dependent methylene-H4F dehydrogenase, NAD-dependent dehydrogenase-cyclohydrolase, NADH-oxidizing methylenetetrahydrofolate reductase, NMDMC
ECTree
1.5.1.15 methylenetetrahydrofolate dehydrogenase (NAD+)Advanced search results
results (
results (Engineering
Engineering on EC 1.5.1.15 - methylenetetrahydrofolate dehydrogenase (NAD+)
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
Q183A
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site-directed mutagenesis, the Gln183Ala variant exhibits a 6-10fold lower rate of folate reduction and bound CH2-H4folate with 7-fold lower affinity compared to wild-type enzyme. The oxidative half-reaction of the Gln183Ala mutant is considered reversible, and the enzyme can catalyze either of two half reactions involving folate: reduction of CH2-H4folate as part of the physiological oxidoreductase reaction or oxidation of CH3-H4folate as part of the CH3-H4folate-menadione oxidoreductase reaction, comparisons of half-reaction kinetics of wild-type and mutant enzymes
Q183E
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site-directed mutagenesis, comparisons of half-reaction kinetics of wild-type and mutant enzymes, the Gln183Glu mutant displays catalytic constants within 3fold of the wild-type enzyme enzyme
C677T
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one of several polymorphisms, leads to increased risk of hepatocellular carcinoma in patients with alcoholic cirrhosis, determination of genotypes in liver transplant patients with cirrhosis with and without hepatocellular carcinoma and in healthy persons
D133A
cosubstrate NAD+, 1.7% of wild-type activity, cosubstrate NADP+, 5.5% of wild-type activity
D133N
cosubstrate NAD+, 20.4% of wild-type activity, cosubstrate NADP+, 82.2% of wild-type activity
D133S
cosubstrate NAD+, 17.8% of wild-type activity, cosubstrate NADP+, 34.5% of wild-type activity
R198A
cosubstrate NAD+, 0.7% of wild-type activity, cosubstrate NADP+, 5.3% of wild-type activity
R198K
cosubstrate NAD+, 56% of wild-type activity, cosubstrate NADP+, 42% of wild-type activity
R198S
cosubstrate NAD+, 0.9% of wild-type activity, cosubstrate NADP+, 53% of wild-type activity
K56Q
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inactivation of methenyltetrahydrofolate cyclohydrolase activity of bifunctional enzyme. Transfection with mutant enzyme rescues auxotrophy of enzyme-deficient fibroblasts, but only poorly. Rescued cells demonstrate a decrease in the ratio of incorporation of exogenous formate to serine
additional information
additional information
construction of a gene deletion mutant cell line, the cells can survive in liver and other tissues because the null defect is rescued by metabolites supplied by surrounding normal cells
additional information
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primary fibroblasts from embryo of knock-out mice, spontaneous immortalization, the mutant cells require methionine and glycine for growth, glycine auxotrophy, replacement of mehtionine by homocysteine results in much lower enzyme activity, metabolism overview
additional information
short hairpin RNAs (shRNAs) suppression of expression of Mthfd2 gene in E14 mouse embryonic stem cells (mESCs). Mthfd2 knockdown (KD) results in loss of typical stem cell morphology, with reduced alkaline phosphatase (AP) staining. The expression of pluripotency marker genes is downregulated and that of lineage marker genes upregulated, showing that Mthfd2 depletion results in differentiation of mESCs. Knockdown of Mthfd2 in another G4 mESC line shows results consistent with those in Mthfd2 KD E14 mESCs. Additionally, homozygous Mthfd2 knockout (KO) mESCs are characterized by the loss of typical mESC morphology, abnormal expression of marker genes, and compromised cell proliferation. Forced expression of Mthfd2 rescues the Mthfd2 KO-induced differentiation and compromised cell proliferation. In addition, MTHFD2 protein expression is gradually silenced during the differentiation of mESCs into embryoid bodies (EBs). Expression of Mthfd2 facilitates mouse induced pluripotent stem cells (iPSCs)induction, Mthfd2 promotes complete reprogramming of iPSCs and improves the quality of iPSCs. All iPSCs induced with Mthfd2 (OSKM2 iPSCs) show typical mESC-like morphology and express Oct4-driven GFP. Analysis of changes in the transcriptome due to suppression of Mthfd2. Mthfd2 depletion hinders DNA repair in mESCs
additional information
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short hairpin RNAs (shRNAs) suppression of expression of Mthfd2 gene in E14 mouse embryonic stem cells (mESCs). Mthfd2 knockdown (KD) results in loss of typical stem cell morphology, with reduced alkaline phosphatase (AP) staining. The expression of pluripotency marker genes is downregulated and that of lineage marker genes upregulated, showing that Mthfd2 depletion results in differentiation of mESCs. Knockdown of Mthfd2 in another G4 mESC line shows results consistent with those in Mthfd2 KD E14 mESCs. Additionally, homozygous Mthfd2 knockout (KO) mESCs are characterized by the loss of typical mESC morphology, abnormal expression of marker genes, and compromised cell proliferation. Forced expression of Mthfd2 rescues the Mthfd2 KO-induced differentiation and compromised cell proliferation. In addition, MTHFD2 protein expression is gradually silenced during the differentiation of mESCs into embryoid bodies (EBs). Expression of Mthfd2 facilitates mouse induced pluripotent stem cells (iPSCs)induction, Mthfd2 promotes complete reprogramming of iPSCs and improves the quality of iPSCs. All iPSCs induced with Mthfd2 (OSKM2 iPSCs) show typical mESC-like morphology and express Oct4-driven GFP. Analysis of changes in the transcriptome due to suppression of Mthfd2. Mthfd2 depletion hinders DNA repair in mESCs
additional information
construction of the Mycobacterium smegmatis DELTAmsmeg_6596 strain. The mutant is partially auxotrophic for methionine and grows only poorly without methionine or without being complemented with a functional copy of MTHFR1 or MTHFR2. Furthermore, the DELTAmsmeg_6596 strain is more sensitive to folate pathway inhibitors (sulfachloropyridazine, p-aminosalicylic acid, sulfamethoxazole, and trimethoprim)
additional information
construction of the Mycobacterium smegmatis DELTAmsmeg_6596 strain. The mutant is partially auxotrophic for methionine and grows only poorly without methionine or without being complemented with a functional copy of MTHFR1 or MTHFR2. Furthermore, the DELTAmsmeg_6596 strain is more sensitive to folate pathway inhibitors (sulfachloropyridazine, p-aminosalicylic acid, sulfamethoxazole, and trimethoprim)
additional information
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construction of the Mycobacterium smegmatis DELTAmsmeg_6596 strain. The mutant is partially auxotrophic for methionine and grows only poorly without methionine or without being complemented with a functional copy of MTHFR1 or MTHFR2. Furthermore, the DELTAmsmeg_6596 strain is more sensitive to folate pathway inhibitors (sulfachloropyridazine, p-aminosalicylic acid, sulfamethoxazole, and trimethoprim)
additional information
-
construction of the Mycobacterium smegmatis DELTAmsmeg_6596 strain. The mutant is partially auxotrophic for methionine and grows only poorly without methionine or without being complemented with a functional copy of MTHFR1 or MTHFR2. Furthermore, the DELTAmsmeg_6596 strain is more sensitive to folate pathway inhibitors (sulfachloropyridazine, p-aminosalicylic acid, sulfamethoxazole, and trimethoprim)
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