tetrahydrofolate


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tetrahydrofolate

H4 folate; a coenzyme derived from the reduction of folic acid through dihydrofolate; an important cofactor in the synthesis of purines.
References in periodicals archive ?
Specific to methotrexate, SNPs in methylene tetrahydrofolate reductase (MTHFR) are consistently associated with enhanced methotrexate-mediated bone marrow toxicity but only poorly correlated, at best, with response to methotrexate therapy.
Nutritional management of homocysteinaemia can be confounded by the presence of a genetic defect in methylene tetrahydrofolate reductase (MTHFR), which is involved in recycling of the active form of folic acid.
If a genetic deficiency in either methylene tetrahydrofolate reductase or cystathionine [beta]-synthetase is identified, it needs to be followed up with a fasting plasma homocysteine level.
For remethylation of homocysteine, a methyl group can be transferred either from N5-methyl tetrahydrofolate (THF) by methionine synthase, or from betaine by betaine homocysteine methyl transferase (BHMT).
MTHFR catalyses NADPH-linked reduction of N (5), (10)-methylene-tetrahydrofolate to N (5)-methylene tetrahydrofolate.
a) [up arrow] [up arrow] Cystathionine [beta]-synthase deficiency N (homocystinuria) (a) Cbl metabolism Adenosyl-Cbl-specific deficiencies Cbl A, (a) Cbl B, (a) and Cbl D-Var2 [up arrow] (b) deficiencies Combined methyl-Cbl and adenosyl-Cbl cbl metabolism Cbl C, (c) Cbl D, (c) and Cbl F (b) [up arrow] deficiencies Methyl-Cbl-specific deficiencies Cbl D-Var1, Cbl E, and Cbl G N deficiencies (b) Met adenosyltransferase I/III deficiency (c) N Adenosylhomocysteine hydrolase deficiency (c) N Glycine N-methyltransferase deficiency (c) N Methylene tetrahydrofolate reductase N deficiency (b) Nutritional Cbl deficiency in mother or N to [up arrow] other Cbl metabolism defect (b) (e.
lupus anticoagulants (LA), IgG / IgM antibodies for anticardiolipin (ACA), [beta]2 glycoprotein 1 ([beta]2GPI) and annexin V, protein C (PC), protein S (PS), antithrombin III (AT III), factor V Leiden (FVL) mutation, prothrombin (PT) gene G20210A, methylene tetrahydrofolate reductase (MTHFR) C 677T, endothelial protein C receptor (EPCR) 23 bp insertion and plasminogen activator inhibitor (PAI-1 4G/5G) polymorphisms.
The best studied association is between polymorphisms in the gene methylene tetrahydrofolate reductase (MTHFR), the enzyme that catalyzes the formation of 5-methyl tetrahydrofolate, a critical methyl donor for a variety of metabolic reactions.
Venous thromboembolic disease and the prothrombin, methylene tetrahydrofolate reductase and factor V genes.
Numerous studies have shown that certain risk factors-including mutations in the factor V (Leiden), factor II (prothrombin) and possibly the methylene tetrahydrofolate reductase (MTHFR) genes-appear to work in combination, increasing the likelihood that a patient will develop venous thrombosis.
Because the influence of cobalamin on As methylation could depend on an adequate supply of 5-methyl tetrahydrofolate (THF), we further examined associations between cobalamin and uAs metabolites by folate status (Table 4).