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1 nzyme, estrogen receptor, androgen receptor, methylenetetrahydrofolate reductase).
2 by MTR), methionine synthase reductase, and methylenetetrahydrofolate reductase.
3 ation were until recently largely limited to methylenetetrahydrofolate reductase.
4 c acid targets including Factor V Leiden and methylenetetrahydrofolate reductase.
5 (SHMT) or at the genes encoding one or both methylenetetrahydrofolate reductases.
6 s low: choline dehydrogenase (CHDH) rs12676, methylenetetrahydrofolate reductase 1 (MTHFD1) rs2236225
7 amide ribonucleotide transformylase (347GG), methylenetetrahydrofolate reductase (1298AC/CC), methion
8 factor V 1691A (Leiden), factor II 20 210A, methylenetetrahydrofolate reductase 667T, type 1 plasmin
9 splant body mass index >or= 25, or carry the methylenetetrahydrofolate reductase 677 TT genotype shou
10 oning regimens, body mass index >or= 25, and methylenetetrahydrofolate reductase 677 TT genotype were
11 point mutation (C677T) in the gene encoding methylenetetrahydrofolate reductase, an enzyme involved
12 perhomocysteinemia secondary to mutations in methylenetetrahydrofolate reductase and cystathionine be
13 cumulate via inactivating mutations in metF (methylenetetrahydrofolate reductase) and luxR (the maste
14 , hemoglobin S, the thermolabile mutation of methylenetetrahydrofolate reductase, and the cystic fibr
15 ystathionine-gamma-lyase, paraxonase 1, 5,10-methylenetetrahydrofolate reductase, betaine:homocystein
17 R506G, factor II (prothrombin) G20210A, and methylenetetrahydrofolate reductase C677T, compared with
18 Other genetic variants (prothrombin 20210A, methylenetetrahydrofolate reductase C677T, factor XIII V
20 receptors; and vascular redox determinants (methylenetetrahydrofolate reductase, endothelial nitric
21 ed serine synthesis competes with the enzyme methylenetetrahydrofolate reductase for methylenetetrahy
23 ene (Factor V Leiden), a variant in the 5,10-methylenetetrahydrofolate reductase gene (MTHFR), and an
25 e +/+ genotype for the C677T mutation in the methylenetetrahydrofolate reductase gene have no increas
26 of the common C677T base substitution in the methylenetetrahydrofolate reductase gene in 110 DNA samp
27 iation of CHD with the C677T mutation of the methylenetetrahydrofolate reductase gene or with 3 mutat
31 brinogen, plasminogen activator inhibitor-1, methylenetetrahydrofolate reductase, glycoprotein Illa,
32 iffer from those of the ferredoxin-dependent methylenetetrahydrofolate reductase isolated from the ho
33 (<301 microg/d) of folate, the substrate for methylenetetrahydrofolate reductase; low intake (<1.8 mg
34 (<1.8 mg/d) of vitamin B2, the cofactor for methylenetetrahydrofolate reductase; low intake (<8.0 mi
35 strain of Escherichia coli that overproduces methylenetetrahydrofolate reductase (MetF) has been cons
36 l6, IVS6 -68C>T, 1122A>G, and 1053C>T); 5,10-methylenetetrahydrofolate reductase (MTHFR 677C>T and 12
37 tatus, DNA methylation, and polymorphisms of methylenetetrahydrofolate reductase (MTHFR 677C-->T and
38 morphic genes involved in folate metabolism--methylenetetrahydrofolate reductase (MTHFR C677T and A12
39 on mutation (C677T) in the gene encoding for methylenetetrahydrofolate reductase (MTHFR) (5-methyltet
42 of a key one-carbon metabolizing gene [i.e., methylenetetrahydrofolate reductase (MTHFR) 677C>T and 1
44 em for 2 polymorphisms with effects on 1-CM, methylenetetrahydrofolate reductase (MTHFR) 677C>T, rs18
45 genes coding for folate pathway enzymes 5,10-methylenetetrahydrofolate reductase (MTHFR) 677C-->T and
46 the combined effects of the TC 776C-->G and methylenetetrahydrofolate reductase (MTHFR) 677C-->T pol
49 n capability is demonstrated by analyzing 96 methylenetetrahydrofolate reductase (MTHFR) alleles in p
51 at either of two folate metabolism enzymes, methylenetetrahydrofolate reductase (MTHFR) and methioni
53 The single nucleotide polymorphism (SNP) methylenetetrahydrofolate reductase (MTHFR) C677T (rs180
67 treatment on outcome in patients with severe methylenetetrahydrofolate reductase (MTHFR) deficiency i
68 d families, each with 2 siblings with severe methylenetetrahydrofolate reductase (MTHFR) deficiency m
71 estigated whether a polymorphism in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene (C677T)
72 ariant form (the C677T genotype) of the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene and ris
73 ly reported that 2 polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene at posi
75 ozygosity for the variant 677T allele in the methylenetetrahydrofolate reductase (MTHFR) gene increas
76 etermine whether the C677T transition in the methylenetetrahydrofolate reductase (MTHFR) gene is asso
78 ions in cystathionine beta-synthase (CBS) or methylenetetrahydrofolate reductase (MTHFR) gene lead to
79 abolism and the 677C-->T polymorphism in the methylenetetrahydrofolate reductase (MTHFR) gene may be
80 at nucleotide 677 (677C-->T) mutation of the methylenetetrahydrofolate reductase (MTHFR) gene may be
82 p of a common polymorphism (667C-->T) of the methylenetetrahydrofolate reductase (MTHFR) gene with th
83 hol intake and 2 common polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene, 677C--
84 is illustrated here using the example of the methylenetetrahydrofolate reductase (MTHFR) gene, homocy
85 ssociation between polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, includ
86 ion of chromosome 1 that contains a putative methylenetetrahydrofolate reductase (MTHFR) gene, which
90 of 30 men varying in age, fertility status, methylenetetrahydrofolate reductase (MTHFR) genotype, an
91 risk factors, C-reactive protein (CRP), and methylenetetrahydrofolate reductase (MTHFR) genotype.
92 0 mother-child dyads in association with the methylenetetrahydrofolate reductase (MTHFR) genotype.
94 e induced by deficiency in a key OCM enzyme, methylenetetrahydrofolate reductase (MTHFR) in Mthfr(+/-
103 her homocysteine or MTX toxicity differed by methylenetetrahydrofolate reductase (MTHFR) or reduced f
108 ions in cystathionine beta-synthase (Cbs) or methylenetetrahydrofolate reductase (Mthfr) results in n
113 with hypertension and stroke, independent of methylenetetrahydrofolate reductase (MTHFR) variants.
114 ymorphism (TT genotype) in the gene encoding methylenetetrahydrofolate reductase (MTHFR) was responsi
115 AS1-VNTR; OR = 2.50, 95% CI: 1.54-4.05); and methylenetetrahydrofolate reductase (MTHFR)(Val/Val) (OR
118 (Mat1a), cystathionine-beta-synthase (Cbs), methylenetetrahydrofolate reductase (Mthfr), adenosyl-ho
120 n B(12) exposure, the activity of the enzyme methylenetetrahydrofolate reductase (MTHFR), and epigene
121 on of polymorphisms in thymidylate synthase, methylenetetrahydrofolate reductase (MTHFR), and VEGF.
123 of a prototypical vitamin-dependent enzyme, methylenetetrahydrofolate reductase (MTHFR), from 564 in
124 several B vitamin-dependent enzymes, such as methylenetetrahydrofolate reductase (MTHFR), methionine
125 combination, decreased transcript levels of methylenetetrahydrofolate reductase (MTHFR), methionine
127 in the following folate-metabolizing genes: methylenetetrahydrofolate reductase (MTHFR), reduced fol
128 in the methionine synthase reductase (MTRR), methylenetetrahydrofolate reductase (MTHFR), serine hydr
134 interact with common pathogenic variants in methylenetetrahydrofolate reductase (MTHFR); the most pr
135 The presence of a nonsynonymous SNP in the methylenetetrahydrofolate reductase (MTHFR)gene was asso
138 e thermolabile mutation (TT genotype) of the methylenetetrahydrofolate reductase (MTHFR; EC 1.5.1.20)
140 mes involved in homocysteine metabolism (ie, methylenetetrahydrofolate reductase [MTHFR] 677C>T and 1
141 onine) and related gene polymorphisms (C677T methylenetetrahydrofolate reductase [MTHFR] and C1420T c
143 D1 G870A (AA) polymorphism (P = 0.0138), and methylenetetrahydrofolate reductase (NAD(P)H) C677T (TT)
144 the cyclin D1 G870A (AA) polymorphism or the methylenetetrahydrofolate reductase (NAD(P)H) C677T (TT)
145 bstitution at nucleo-tide 677 (677C-->T)] in methylenetetrahydrofolate reductase (NADPH) and the cofa
146 mouse models of homocystinuria due to either methylenetetrahydrofolate reductase or Met synthase defi
147 deficiencies in cystathionine beta synthase, methylenetetrahydrofolate reductase, or in enzymes invol
149 igned to usual care or GERA, which evaluated methylenetetrahydrofolate reductase polymorphisms and se
151 which acts as an allosteric inhibitor of the methylenetetrahydrofolate reductase reaction and as an a
152 ual disease (hazard ratio 7.3; P < .001) and methylenetetrahydrofolate reductase rs1801131 (hazard ra
153 pathway (i.e. folate or B12 deficiencies or methylenetetrahydrofolate reductase thermolability).