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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 (
26        We have investigated the ability of 5-methyltetrahydrofolate (5-MTHF) and tetrahydrobiopterin
27                       We identified FA and 5-methyltetrahydrofolate (5-mTHF) by retention time and ch
28                Plasma MTX, leucovorin, and 5-methyltetrahydrofolate (5-mTHF) concentrations were meas
29  to release folic acid (FA) and endogenous 5-methyltetrahydrofolate (5-MTHF) from infant milk formula
30 ith normal serum folate levels and low CSF 5-methyltetrahydrofolate (5-MTHF) levels.
31        The circulating form of folic acid, 5-methyltetrahydrofolate (5-MTHF), may have beneficial eff
32 as to analyze the long-term effects of FO, 5-methyltetrahydrofolate (5-MTHF), or FO+5-MTHF prenatal s
33                        We demonstrate that 5-methyltetrahydrofolate (5-MTHF, the predominant folate i
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
38 to circulating unmetabolized folic acid or 5-methyltetrahydrofolate (5MeTHF).
39                              Data on serum 5-methyltetrahydrofolate (5MTHF) and folic acid (FA) conce
40 rent forms of folate, folic acid (FA), and 5-methyltetrahydrofolate (5mTHF), at concentrations of 5 m
41 ssociated with elevated serine but reduced 5-methyltetrahydrofolate (5MTHF).
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
51 synthesizing serine, and (3) it sequesters 5-methyltetrahydrofolate and inhibits SAM synthesis.
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
56                                      Serum 5-methyltetrahydrofolate and vitamin B-12 concentrations w
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
62 a cobalamin-dependent reaction that utilizes methyltetrahydrofolate as a methyl group donor.
63 alyzes the methylation of homocysteine using methyltetrahydrofolate as the methyl donor.
64         We evaluated whether a high-dose L-5-methyltetrahydrofolate-based regimen provided improved t
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
72 rsion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate by MTHFR.
73 alyzes the transfer of methyl groups between methyltetrahydrofolate (CH(3)-H(4)folate) and homocystei
74                                          The methyltetrahydrofolate (CH(3)-H(4)folate) corrinoid-iron
75                                           N5-Methyltetrahydrofolate (CH(3)-H(4)folate) donates a meth
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
82 the folate (Fol) domain for remethylation by methyltetrahydrofolate (CH(3)-H(4)folate).
83 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate).
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.
86           The cobalt center is methylated by methyltetrahydrofolate (CH3-H4folate) to form a methylco
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
89 ein (C/Fe-SP) by the N5 methyl group of (6S)-methyltetrahydrofolate (CH3-H4folate).
90 cantly correlated with cerebrospinal fluid 5-methyltetrahydrofolate concentrations, which were below
91                                          The methyltetrahydrofolate:corrinoid/iron-sulfur protein met
92                                          The methyltetrahydrofolate:corrinoid/iron-sulfur protein met
93                                          The methyltetrahydrofolate:corrinoid/iron-sulfur protein met
94 the cell surface and increases the rate of 5-methyltetrahydrofolate delivery.
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.
97 tetrahydrofolate reductase (MTHFR) generates methyltetrahydrofolate for methylation reactions.
98 ethylation with [(2)H(2)]methyl groups (as 5-methyltetrahydrofolate) formed only from cytosolic proce
99     This protein accepts a methyl group from methyltetrahydrofolate forming Me-Co(3+)CFeSP that then
100 biological circulating folate derivatives, 5-methyltetrahydrofolate, from folate receptors.
101 de SAH hydrolase, methionyl-tRNA synthase, 5-methyltetrahydrofolate:Hcy methyltransferase, S-adenosyl
102                              Transport of N5-methyltetrahydrofolate in human retinal pigment epitheli
103 ve been found necessary for potocytosis of 5-methyltetrahydrofolate in MA104.
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
112  anion exchanger that mediates delivery of 5-methyltetrahydrofolate into mammalian cells.
113 acteristics of the uptake of radiolabeled N5-methyltetrahydrofolate into the cells were investigated.
114                              Transport of N5-methyltetrahydrofolate into these cells occurred by a si
115                                            5-Methyltetrahydrofolate is a major methyl donor in the re
116                          In contrast, when 5-methyltetrahydrofolate is depleted by alcohol consumptio
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
119        A cyclic voltammetry study of 1mM l-5-methyltetrahydrofolate (l-5-MTHF) was performed in pH 5.
120  stability of free and microencapsulated L-5-methyltetrahydrofolate (L-5-MTHF) with free folic acid (
121       Human cDNAs for methionine synthase (5-methyltetrahydrofolate:L-homocysteine S-transmethylase;
122 HF was inhibited by the structural analogs 5-methyltetrahydrofolate, methotrexate and folic acid (K(i
123                                   Although 5-methyltetrahydrofolate (methylTHF) was higher in materna
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
126 essed by determining the uptake of [3H]-N(5)-methyltetrahydrofolate (MTF).
127 or an equimolar amount (17 mg/d) of oral L-5-methyltetrahydrofolate (MTHF group).
128 lly pure 6R- and 6S-3'-aza-2'-(18)F-fluoro-5-methyltetrahydrofolate (MTHF) (6R-(18)F-1 and 6S-(18)F-1
129         The 6R and 6S isomers of (18)F-aza-5-methyltetrahydrofolate (MTHF) were assessed regarding th
130               The main vacuolar folate was 5-methyltetrahydrofolate, of which 51% was polyglutamylate
131 e folate was vacuolar and was again mainly 5-methyltetrahydrofolate, of which 76% was polyglutamylate
132 oss of activity is slowed in the presence of methyltetrahydrofolate or adenosylmethionine.
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
135                                            5-Methyltetrahydrofolate polyglutamates were the only fola
136                                            5-Methyltetrahydrofolate, SAM, and SAM/S-adenosylhomocyste
137                   Especially in faba bean, 5-methyltetrahydrofolate showed surprisingly good stabilit
138 rmal proportions of one-carbon forms, with 5-methyltetrahydrofolate the most abundant, but were less
139 ficiency via the accumulation of folate as 5-methyltetrahydrofolate (the "methyl trap").
140                These studies, done with N(5)-methyltetrahydrofolate (the predominant folate derivativ
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
144       MTHFR null mutants (mthfr(-)) lacked 5-methyltetrahydrofolate, the most abundant intracellular
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
151 methylcobalamin to homocysteine but not from methyltetrahydrofolate to free cob(I)alamin.
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
163 the protein to catalyze methyl transfer from methyltetrahydrofolate to homocysteine.
164 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine.
165 ntermediate carrier of the methyl group from methyltetrahydrofolate to homocysteine.
166         MetF also catalyzes the oxidation of methyltetrahydrofolate to methylenetetrahydrofolate in t
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
170                         In contrast, binding methyltetrahydrofolate to the enzyme does not result in
171 group that is in transit from one substrate (methyltetrahydrofolate) to another (homocysteine).
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
174       In addition, the characteristics of N5-methyltetrahydrofolate uptake in these cells were compar
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
182              This reaction is regulated by 5-methyltetrahydrofolate, which inhibits the enzyme cataly
183  sole enzyme responsible for generation of 5-methyltetrahydrofolate, which is required for methionine

 
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