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1 cal amounts of FA or the reduced folate, L-5-methyltetrahydrofolate.
2 revent excessive conversion of methylene- to methyltetrahydrofolate.
3 ction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate.
4 inding of folic acid and by the uptake of N5-methyltetrahydrofolate.
5 hionine and flavodoxin but unreactive toward methyltetrahydrofolate.
6 The cofactor is then remethylated by methyltetrahydrofolate.
7 nzyme activity, leading to lower levels of 5-methyltetrahydrofolate.
8 for the (6S) and (6R) diastereoisomers of N5-methyltetrahydrofolate.
9 the receptor in the observed transport of N5-methyltetrahydrofolate.
10 talyze methylation of free cob(I)alamin with methyltetrahydrofolate.
11 ate than the reactions with homocysteine and methyltetrahydrofolate.
12 e conversion of methylenetetrahydrofolate to methyltetrahydrofolate.
13 methionine using a methyl group derived from methyltetrahydrofolate.
14 ated to form l-methionine by betaine or N(5)-methyltetrahydrofolate.
15 ystal structure of rat GNMT complexed with 5-methyltetrahydrofolate.
16 is inhibited by a specific form of folate, 5-methyltetrahydrofolate.
17 hionine by using a methyl group derived from methyltetrahydrofolate.
18 ation from MtvC to tetrahydrofolate, forming methyltetrahydrofolate.
19 late; and (3) determination of total liver 5-methyltetrahydrofolate.
20 method involves (1) determination of liver 5-methyltetrahydrofolate; (2) chemical reduction of liver
21 The pH dependence of the uptake of [(3)H]-methyltetrahydrofolate ([(3)H]-MTF) was assayed in Mulle
22 for the circulating folate coenzyme, (6S)-5-methyltetrahydrofolate (5-CH3H4folate), and its opposite
23 y trapping folate cofactors in the form of 5-methyltetrahydrofolate (5-methylTHF) and subsequent inhi
24 ductase (MTHFR) catalyzes the synthesis of 5-methyltetrahydrofolate (5-methylTHF), the methyl donor f
25 otal folate and individual folate vitamer [5-methyltetrahydrofolate (5-methylTHF), unmetabolized FA (
29 to release folic acid (FA) and endogenous 5-methyltetrahydrofolate (5-MTHF) from infant milk formula
32 as to analyze the long-term effects of FO, 5-methyltetrahydrofolate (5-MTHF), or FO+5-MTHF prenatal s
34 licitation of different forms of folates - 5-methyltetrahydrofolate, 5-formyltetrahydrofolate and 10-
35 ations of folic acid, 10-formylfolic acid, 5-methyltetrahydrofolate, 5-formyltetrahydrofolate and tet
36 rmination and high enzymatic production of 5-methyltetrahydrofolate, 5-formyltetrahydrofolate and tet
37 ween maternal folate status as measured by 5-methyltetrahydrofolate (5MeTHF), 5-formyltetrahydrofolat
40 rent forms of folate, folic acid (FA), and 5-methyltetrahydrofolate (5mTHF), at concentrations of 5 m
42 old) greater relative affinities for (6S)-N5-methyltetrahydrofolate, (6S)-N5-formyltetrahydrofolate a
43 thylenetetrahydrofolate reductase (MTHFR) (5-methyltetrahydrofolate:(acceptor) oxidoreductase, EC 1.7
44 f the folate derivatives demonstrated that 5-methyltetrahydrofolate accounts for 30% of total cellula
45 be involved in the binding and activation of methyltetrahydrofolate, amino acids 650-896 are responsi
46 lded predominantly polyglutamates of [(3)H]5-methyltetrahydrofolate and [(3)H]5-formyltetrahydrofolat
47 cysteine is dependent on the production of 5-methyltetrahydrofolate and adequate vitamin B-12 for the
48 derstanding the biochemical balance in using methyltetrahydrofolate and betaine as methyl donors as w
49 mics and kinetics of methyl transfer between methyltetrahydrofolate and cob(I)alamin or cob(I)inamide
50 the cobalamin is alternatively methylated by methyltetrahydrofolate and demethylated by homocysteine
52 lNC females had higher BW and lower plasma 5-methyltetrahydrofolate and methionine consistent with lo
53 was specific for such reduced folates as N5-methyltetrahydrofolate and N5-formyltetrahydrofolate.
54 yzes the methylation of free cob(I)alamin by methyltetrahydrofolate and the methylation of homocystei
55 sources that lead to the production of N(5)-methyltetrahydrofolate and the remethylation of l-homocy
57 to 10-fold, 3) did not change affinity for 5-methyltetrahydrofolate, and 4) except for E45R decreased
58 ion of free folic acid, tetrahydrofolate, 5'-methyltetrahydrofolate, and 5'-formyltetrahydrofolate in
59 The LOQ and LOD for tetrahydrofolate, 5'-methyltetrahydrofolate, and 5'-formyltetrahydrofolate we
60 th three different substrates: homocysteine, methyltetrahydrofolate, and S-adenosyl-l-methionine (Ado
61 etetrahydrofolate (stabilized at pH 10) to 5-methyltetrahydrofolate; and (3) determination of total l
65 to high-dose folic acid, high-dose oral L-5-methyltetrahydrofolate-based supplementation does not af
66 nterconversion of all folate vitamers into 5-methyltetrahydrofolate before 14 h of germination and hi
67 ocysteine binding region (residues 2-353), a methyltetrahydrofolate binding region (residues 354-649)
68 ent manner, and (2) cSHMT, a high affinity 5-methyltetrahydrofolate-binding protein, sequesters this
69 pathway by transferring a methyl group from methyltetrahydrofolate bound to a methyltransferase to t
70 chloroplasts and lowered the proportion of 5-methyltetrahydrofolate but did not discernibly affect gr
71 ion, the enzyme reacts with homocysteine and methyltetrahydrofolate but is unreactive toward adenosyl
73 alyzes the transfer of methyl groups between methyltetrahydrofolate (CH(3)-H(4)folate) and homocystei
76 lyzes the transfer of the N5-methyl group of methyltetrahydrofolate (CH(3)-H(4)folate) to the sulfur
77 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate) using flavin a
78 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate) using flavin a
79 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate) using NADH as
80 thesis of methionine from homocysteine and 5-methyltetrahydrofolate (CH(3)-H(4)folate) using the uniq
81 enetetrahydrofolate (CH(2)-H(4)folate) to N5-methyltetrahydrofolate (CH(3)-H(4)folate), committing a
84 nthesis using the triglutamate derivative of methyltetrahydrofolate (CH(3)-H(4)PteGlu(3)) as methyl d
85 ntinuous transmethylation of homocysteine by methyltetrahydrofolate (CH(3)THF) to form methionine.
87 yzes transfer of the N5-methyl group of (6S)-methyltetrahydrofolate (CH3-H4folate) to the cob(I)amide
88 es transfer of the N5-methyl group from (6S)-methyltetrahydrofolate (CH3-H4folate) to the cobalt cent
90 cantly correlated with cerebrospinal fluid 5-methyltetrahydrofolate concentrations, which were below
95 cob(I)alamin cofactor: methyl transfer from methyltetrahydrofolate during primary turnover and methy
96 smegmatis utilization of monoglutamylated 5-methyltetrahydrofolate exogenously added to the medium.
98 ethylation with [(2)H(2)]methyl groups (as 5-methyltetrahydrofolate) formed only from cytosolic proce
101 de SAH hydrolase, methionyl-tRNA synthase, 5-methyltetrahydrofolate:Hcy methyltransferase, S-adenosyl
104 an (+/- SEM) rate of appearance of [(13)C5]5-methyltetrahydrofolate in plasma was 0.33 +/- 0.09 (capl
105 tep in the pathway, but also tightly binds 5-methyltetrahydrofolate in the cytoplasm, a required cofa
106 rculating concentrations of folic acid and 5-methyltetrahydrofolate in the Framingham Offspring Cohor
107 steady-state reactions with homocysteine and methyltetrahydrofolate in the presence of phenol red, we
108 mount (17 mg/day) of the reduced folate, L-5-methyltetrahydrofolate, in addition to 50.0 mg/day of vi
109 Folic acid and its active metabolite, 5-methyltetrahydrofolate, increase endothelium-dependent v
110 olate and its derivatives methotrexate and 5-methyltetrahydrofolate induced H(+)-coupled inward curre
111 ethotrexate, 5-formyltetrahydrofolate, and 5-methyltetrahydrofolate initial rates and net uptake in c
113 acteristics of the uptake of radiolabeled N5-methyltetrahydrofolate into the cells were investigated.
117 ant route by which the major blood folate, 5-methyltetrahydrofolate, is transported into mammalian ce
118 emperature to study the stability of 1mM l-5-methyltetrahydrofolate (l-5-MTHF) in combination with ep
120 stability of free and microencapsulated L-5-methyltetrahydrofolate (L-5-MTHF) with free folic acid (
122 HF was inhibited by the structural analogs 5-methyltetrahydrofolate, methotrexate and folic acid (K(i
124 hylating dUMP to dTMP in DNA synthesis, to 5-methyltetrahydrofolate (methylTHF), the primary methyl d
125 throughout treatment and concentrations of 5-methyltetrahydrofolate (MTF), methionine (MET), SAM, and
128 lly pure 6R- and 6S-3'-aza-2'-(18)F-fluoro-5-methyltetrahydrofolate (MTHF) (6R-(18)F-1 and 6S-(18)F-1
131 e folate was vacuolar and was again mainly 5-methyltetrahydrofolate, of which 76% was polyglutamylate
133 t of pemetrexed; influx of folic acid, (6S)5-methyltetrahydrofolate, or (6S)5-formyltetrahydrofolate
134 of the folate increase was contributed by 5-methyltetrahydrofolate polyglutamates and 5,10-methenylt
138 rmal proportions of one-carbon forms, with 5-methyltetrahydrofolate the most abundant, but were less
141 ahydrofolate reductase (MTHFR) synthesizes 5-methyltetrahydrofolate, the major carbon donor in remeth
142 e conversion of methylenetetrahydrofolate to methyltetrahydrofolate, the major methyl donor for the c
143 he reduction of methylenetetrahydrofolate to methyltetrahydrofolate, the methyl donor for the convers
145 ction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, the predominant circulatory form
146 red for purine and thymidine syntheses, to 5-methyltetrahydrofolate, the primary circulatory form of
147 onine and cob(I)alamin enzyme, and then from methyltetrahydrofolate to cob(I)alamin enzyme, generatin
148 the ability to catalyze methyl transfer from methyltetrahydrofolate to exogenous cob(I)alamin, but ha
149 teine but do not affect methyl transfer from methyltetrahydrofolate to exogenous cob(I)alamin, consis
150 ar protein that is alternately methylated by methyltetrahydrofolate to form methylcobalamin and demet
152 et reaction, transfer of a methyl group from methyltetrahydrofolate to homocysteine (Hcy) to form met
153 se catalyzes a methyl transfer reaction from methyltetrahydrofolate to homocysteine to form methionin
154 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine to form methionin
155 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine to form tetrahydr
156 in which a methyl group is transferred from methyltetrahydrofolate to homocysteine to generate tetra
157 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine to give tetrahydr
158 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine to produce methio
159 that catalyzes a methyl group transfer from methyltetrahydrofolate to homocysteine via a methylcob(I
160 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine via the enzyme-bo
161 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine, forming tetrahyd
162 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine, generating tetra
167 this, leaf tissues metabolized [methyl-(14)C]methyltetrahydrofolate to serine, sugars, and starch.
168 ric methods are based on the conversion of 5-methyltetrahydrofolate to tetrahydrofolate by methionine
169 e enzyme then catalyzes methyl transfer from methyltetrahydrofolate to the cob(I)alamin cofactor, for
172 itamin D(3)], folate vitamers (folic acid, 5-methyltetrahydrofolate, total folates), and fatty acids
173 cells do not contain detectable levels of 5-methyltetrahydrofolate under the same culture conditions
175 ction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, used to methylate homocysteine i
176 he reduction of methylenetetrahydrofolate to methyltetrahydrofolate, using NADH as the reductant.
177 hydrofolate reductase (MTHFR), synthesizes 5-methyltetrahydrofolate, utilized in homocysteine remethy
178 tains the regions that bind homocysteine and methyltetrahydrofolate utilizes exogenously supplied cob
179 ynthesis of methionine from homocysteine and methyltetrahydrofolate via two methyl transfer reactions
180 The folate receptor-mediated transport of 5-methyltetrahydrofolate was almost completely blocked in
181 receptor-mediated transport of [3H]-(6S)-N5-methyltetrahydrofolate was much more efficient in L1210A
183 sole enzyme responsible for generation of 5-methyltetrahydrofolate, which is required for methionine