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