ライフサイエンスコーパス: methyltetrahydrofolate

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 methionine using a methyl group derived from methyltetrahydrofolate.

13 ated to form l-methionine by betaine or N(5)-methyltetrahydrofolate.

14 ystal structure of rat GNMT complexed with 5-methyltetrahydrofolate.

15 is inhibited by a specific form of folate, 5-methyltetrahydrofolate.

16 hionine by using a methyl group derived from methyltetrahydrofolate.

17 ation from MtvC to tetrahydrofolate, forming methyltetrahydrofolate.

18 late; and (3) determination of total liver 5-methyltetrahydrofolate.

19 method involves (1) determination of liver 5-methyltetrahydrofolate; (2) chemical reduction of liver

20 The pH dependence of the uptake of [(3)H]-methyltetrahydrofolate ([(3)H]-MTF) was assayed in Mulle

21 for the circulating folate coenzyme, (6S)-5-methyltetrahydrofolate (5-CH3H4folate), and its opposite

22 y trapping folate cofactors in the form of 5-methyltetrahydrofolate (5-methylTHF) and subsequent inhi

23 ductase (MTHFR) catalyzes the synthesis of 5-methyltetrahydrofolate (5-methylTHF), the methyl donor f

24 We have investigated the ability of 5-methyltetrahydrofolate (5-MTHF) and tetrahydrobiopterin

25 We identified FA and 5-methyltetrahydrofolate (5-mTHF) by retention time and ch

26 Plasma MTX, leucovorin, and 5-methyltetrahydrofolate (5-mTHF) concentrations were meas

27 to release folic acid (FA) and endogenous 5-methyltetrahydrofolate (5-MTHF) from infant milk formula

28 ith normal serum folate levels and low CSF 5-methyltetrahydrofolate (5-MTHF) levels.

29 The circulating form of folic acid, 5-methyltetrahydrofolate (5-MTHF), may have beneficial eff

30 as to analyze the long-term effects of FO, 5-methyltetrahydrofolate (5-MTHF), or FO+5-MTHF prenatal s

31 We demonstrate that 5-methyltetrahydrofolate (5-MTHF, the predominant folate i

32 licitation of different forms of folates - 5-methyltetrahydrofolate, 5-formyltetrahydrofolate and 10-

33 ween maternal folate status as measured by 5-methyltetrahydrofolate (5MeTHF), 5-formyltetrahydrofolat

34 to circulating unmetabolized folic acid or 5-methyltetrahydrofolate (5MeTHF).

35 Data on serum 5-methyltetrahydrofolate (5MTHF) and folic acid (FA) conce

36 old) greater relative affinities for (6S)-N5-methyltetrahydrofolate, (6S)-N5-formyltetrahydrofolate a

37 thylenetetrahydrofolate reductase (MTHFR) (5-methyltetrahydrofolate:(acceptor) oxidoreductase, EC 1.7

38 f the folate derivatives demonstrated that 5-methyltetrahydrofolate accounts for 30% of total cellula

39 be involved in the binding and activation of methyltetrahydrofolate, amino acids 650-896 are responsi

40 lded predominantly polyglutamates of [(3)H]5-methyltetrahydrofolate and [(3)H]5-formyltetrahydrofolat

41 cysteine is dependent on the production of 5-methyltetrahydrofolate and adequate vitamin B-12 for the

42 derstanding the biochemical balance in using methyltetrahydrofolate and betaine as methyl donors as w

43 mics and kinetics of methyl transfer between methyltetrahydrofolate and cob(I)alamin or cob(I)inamide

44 the cobalamin is alternatively methylated by methyltetrahydrofolate and demethylated by homocysteine

45 synthesizing serine, and (3) it sequesters 5-methyltetrahydrofolate and inhibits SAM synthesis.

46 was specific for such reduced folates as N5-methyltetrahydrofolate and N5-formyltetrahydrofolate.

47 yzes the methylation of free cob(I)alamin by methyltetrahydrofolate and the methylation of homocystei

48 sources that lead to the production of N(5)-methyltetrahydrofolate and the remethylation of l-homocy

49 Serum 5-methyltetrahydrofolate and vitamin B-12 concentrations w

50 to 10-fold, 3) did not change affinity for 5-methyltetrahydrofolate, and 4) except for E45R decreased

51 ion of free folic acid, tetrahydrofolate, 5'-methyltetrahydrofolate, and 5'-formyltetrahydrofolate in

52 The LOQ and LOD for tetrahydrofolate, 5'-methyltetrahydrofolate, and 5'-formyltetrahydrofolate we

53 th three different substrates: homocysteine, methyltetrahydrofolate, and S-adenosyl-l-methionine (Ado

54 etetrahydrofolate (stabilized at pH 10) to 5-methyltetrahydrofolate; and (3) determination of total l

55 a cobalamin-dependent reaction that utilizes methyltetrahydrofolate as a methyl group donor.

56 alyzes the methylation of homocysteine using methyltetrahydrofolate as the methyl donor.

57 We evaluated whether a high-dose L-5-methyltetrahydrofolate-based regimen provided improved t

58 to high-dose folic acid, high-dose oral L-5-methyltetrahydrofolate-based supplementation does not af

59 ocysteine binding region (residues 2-353), a methyltetrahydrofolate binding region (residues 354-649)

60 ent manner, and (2) cSHMT, a high affinity 5-methyltetrahydrofolate-binding protein, sequesters this

61 pathway by transferring a methyl group from methyltetrahydrofolate bound to a methyltransferase to t

62 chloroplasts and lowered the proportion of 5-methyltetrahydrofolate but did not discernibly affect gr

63 ion, the enzyme reacts with homocysteine and methyltetrahydrofolate but is unreactive toward adenosyl

64 rsion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate by MTHFR.

65 alyzes the transfer of methyl groups between methyltetrahydrofolate (CH(3)-H(4)folate) and homocystei

66 The methyltetrahydrofolate (CH(3)-H(4)folate) corrinoid-iron

67 N5-Methyltetrahydrofolate (CH(3)-H(4)folate) donates a meth

68 lyzes the transfer of the N5-methyl group of methyltetrahydrofolate (CH(3)-H(4)folate) to the sulfur

69 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate) using flavin a

70 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate) using flavin a

71 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate) using NADH as

72 the folate (Fol) domain for remethylation by methyltetrahydrofolate (CH(3)-H(4)folate).

73 lenetetrahydrofolate (CH(2)-H(4)folate) to 5-methyltetrahydrofolate (CH(3)-H(4)folate).

74 nthesis using the triglutamate derivative of methyltetrahydrofolate (CH(3)-H(4)PteGlu(3)) as methyl d

75 The cobalt center is methylated by methyltetrahydrofolate (CH3-H4folate) to form a methylco

76 yzes transfer of the N5-methyl group of (6S)-methyltetrahydrofolate (CH3-H4folate) to the cob(I)amide

77 es transfer of the N5-methyl group from (6S)-methyltetrahydrofolate (CH3-H4folate) to the cobalt cent

78 ein (C/Fe-SP) by the N5 methyl group of (6S)-methyltetrahydrofolate (CH3-H4folate).

79 cantly correlated with cerebrospinal fluid 5-methyltetrahydrofolate concentrations, which were below

80 The methyltetrahydrofolate:corrinoid/iron-sulfur protein met

81 The methyltetrahydrofolate:corrinoid/iron-sulfur protein met

82 The methyltetrahydrofolate:corrinoid/iron-sulfur protein met

83 the cell surface and increases the rate of 5-methyltetrahydrofolate delivery.

84 cob(I)alamin cofactor: methyl transfer from methyltetrahydrofolate during primary turnover and methy

85 smegmatis utilization of monoglutamylated 5-methyltetrahydrofolate exogenously added to the medium.

86 tetrahydrofolate reductase (MTHFR) generates methyltetrahydrofolate for methylation reactions.

87 ethylation with [(2)H(2)]methyl groups (as 5-methyltetrahydrofolate) formed only from cytosolic proce

88 This protein accepts a methyl group from methyltetrahydrofolate forming Me-Co(3+)CFeSP that then

89 de SAH hydrolase, methionyl-tRNA synthase, 5-methyltetrahydrofolate:Hcy methyltransferase, S-adenosyl

90 Transport of N5-methyltetrahydrofolate in human retinal pigment epitheli

91 ve been found necessary for potocytosis of 5-methyltetrahydrofolate in MA104.

92 an (+/- SEM) rate of appearance of [(13)C5]5-methyltetrahydrofolate in plasma was 0.33 +/- 0.09 (capl

93 tep in the pathway, but also tightly binds 5-methyltetrahydrofolate in the cytoplasm, a required cofa

94 rculating concentrations of folic acid and 5-methyltetrahydrofolate in the Framingham Offspring Cohor

95 steady-state reactions with homocysteine and methyltetrahydrofolate in the presence of phenol red, we

96 mount (17 mg/day) of the reduced folate, L-5-methyltetrahydrofolate, in addition to 50.0 mg/day of vi

97 Folic acid and its active metabolite, 5-methyltetrahydrofolate, increase endothelium-dependent v

98 olate and its derivatives methotrexate and 5-methyltetrahydrofolate induced H(+)-coupled inward curre

99 ethotrexate, 5-formyltetrahydrofolate, and 5-methyltetrahydrofolate initial rates and net uptake in c

100 anion exchanger that mediates delivery of 5-methyltetrahydrofolate into mammalian cells.

101 acteristics of the uptake of radiolabeled N5-methyltetrahydrofolate into the cells were investigated.

102 Transport of N5-methyltetrahydrofolate into these cells occurred by a si

103 5-Methyltetrahydrofolate is a major methyl donor in the re

104 In contrast, when 5-methyltetrahydrofolate is depleted by alcohol consumptio

105 ant route by which the major blood folate, 5-methyltetrahydrofolate, is transported into mammalian ce

106 emperature to study the stability of 1mM l-5-methyltetrahydrofolate (l-5-MTHF) in combination with ep

107 A cyclic voltammetry study of 1mM l-5-methyltetrahydrofolate (l-5-MTHF) was performed in pH 5.

108 stability of free and microencapsulated L-5-methyltetrahydrofolate (L-5-MTHF) with free folic acid (

109 Human cDNAs for methionine synthase (5-methyltetrahydrofolate:L-homocysteine S-transmethylase;

110 HF was inhibited by the structural analogs 5-methyltetrahydrofolate, methotrexate and folic acid (K(i

111 Although 5-methyltetrahydrofolate (methylTHF) was higher in materna

112 hylating dUMP to dTMP in DNA synthesis, to 5-methyltetrahydrofolate (methylTHF), the primary methyl d

113 throughout treatment and concentrations of 5-methyltetrahydrofolate (MTF), methionine (MET), SAM, and

114 essed by determining the uptake of [3H]-N(5)-methyltetrahydrofolate (MTF).

115 or an equimolar amount (17 mg/d) of oral L-5-methyltetrahydrofolate (MTHF group).

116 The main vacuolar folate was 5-methyltetrahydrofolate, of which 51% was polyglutamylate

117 e folate was vacuolar and was again mainly 5-methyltetrahydrofolate, of which 76% was polyglutamylate

118 oss of activity is slowed in the presence of methyltetrahydrofolate or adenosylmethionine.

119 t of pemetrexed; influx of folic acid, (6S)5-methyltetrahydrofolate, or (6S)5-formyltetrahydrofolate

120 of the folate increase was contributed by 5-methyltetrahydrofolate polyglutamates and 5,10-methenylt

121 5-Methyltetrahydrofolate polyglutamates were the only fola

122 5-Methyltetrahydrofolate, SAM, and SAM/S-adenosylhomocyste

123 rmal proportions of one-carbon forms, with 5-methyltetrahydrofolate the most abundant, but were less

124 ficiency via the accumulation of folate as 5-methyltetrahydrofolate (the "methyl trap").

125 These studies, done with N(5)-methyltetrahydrofolate (the predominant folate derivativ

126 ahydrofolate reductase (MTHFR) synthesizes 5-methyltetrahydrofolate, the major carbon donor in remeth

127 e conversion of methylenetetrahydrofolate to methyltetrahydrofolate, the major methyl donor for the c

128 he reduction of methylenetetrahydrofolate to methyltetrahydrofolate, the methyl donor for the convers

129 MTHFR null mutants (mthfr(-)) lacked 5-methyltetrahydrofolate, the most abundant intracellular

130 ction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, the predominant circulatory form

131 red for purine and thymidine syntheses, to 5-methyltetrahydrofolate, the primary circulatory form of

132 onine and cob(I)alamin enzyme, and then from methyltetrahydrofolate to cob(I)alamin enzyme, generatin

133 the ability to catalyze methyl transfer from methyltetrahydrofolate to exogenous cob(I)alamin, but ha

134 teine but do not affect methyl transfer from methyltetrahydrofolate to exogenous cob(I)alamin, consis

135 ar protein that is alternately methylated by methyltetrahydrofolate to form methylcobalamin and demet

136 methylcobalamin to homocysteine but not from methyltetrahydrofolate to free cob(I)alamin.

137 et reaction, transfer of a methyl group from methyltetrahydrofolate to homocysteine (Hcy) to form met

138 se catalyzes a methyl transfer reaction from methyltetrahydrofolate to homocysteine to form methionin

139 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine to form tetrahydr

140 in which a methyl group is transferred from methyltetrahydrofolate to homocysteine to generate tetra

141 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine to give tetrahydr

142 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine to produce methio

143 that catalyzes a methyl group transfer from methyltetrahydrofolate to homocysteine via a methylcob(I

144 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine via the enzyme-bo

145 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine, forming tetrahyd

146 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine, generating tetra

147 the protein to catalyze methyl transfer from methyltetrahydrofolate to homocysteine.

148 atalyzes the transfer of a methyl group from methyltetrahydrofolate to homocysteine.

149 ntermediate carrier of the methyl group from methyltetrahydrofolate to homocysteine.

150 MetF also catalyzes the oxidation of methyltetrahydrofolate to methylenetetrahydrofolate in t

151 this, leaf tissues metabolized [methyl-(14)C]methyltetrahydrofolate to serine, sugars, and starch.

152 ric methods are based on the conversion of 5-methyltetrahydrofolate to tetrahydrofolate by methionine

153 e enzyme then catalyzes methyl transfer from methyltetrahydrofolate to the cob(I)alamin cofactor, for

154 In contrast, binding methyltetrahydrofolate to the enzyme does not result in

155 group that is in transit from one substrate (methyltetrahydrofolate) to another (homocysteine).

156 cells do not contain detectable levels of 5-methyltetrahydrofolate under the same culture conditions

157 In addition, the characteristics of N5-methyltetrahydrofolate uptake in these cells were compar

158 ction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, used to methylate homocysteine i

159 he reduction of methylenetetrahydrofolate to methyltetrahydrofolate, using NADH as the reductant.

160 hydrofolate reductase (MTHFR), synthesizes 5-methyltetrahydrofolate, utilized in homocysteine remethy

161 tains the regions that bind homocysteine and methyltetrahydrofolate utilizes exogenously supplied cob

162 ynthesis of methionine from homocysteine and methyltetrahydrofolate via two methyl transfer reactions

163 The folate receptor-mediated transport of 5-methyltetrahydrofolate was almost completely blocked in

164 receptor-mediated transport of [3H]-(6S)-N5-methyltetrahydrofolate was much more efficient in L1210A

165 This reaction is regulated by 5-methyltetrahydrofolate, which inhibits the enzyme cataly

166 sole enzyme responsible for generation of 5-methyltetrahydrofolate, which is required for methionine