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1 folates as N5-methyltetrahydrofolate and N5-formyltetrahydrofolate.
2 pemetrexed activity in growth medium with 5-formyltetrahydrofolate.
3 a complex with uridine monophosphate and N-5-formyltetrahydrofolate.
4 conversion of methenyltetrahydrofolate to 5-formyltetrahydrofolate.
5 ersion of 5,10-methenyltetrahydrofolate to 5-formyltetrahydrofolate.
6 as catalytically inactive and did not bind 5-formyltetrahydrofolate.
7 lysis of 5, 10-methenyltetrahydrofolate to 5-formyltetrahydrofolate.
8 s the reversible ATP-driven production of 10-formyltetrahydrofolate (10-formyl-H(4)PteGlu(n)) from fo
9 (MTF) located in mitochondria and uses N(10)-formyltetrahydrofolate (10-formyl-THF) as the formyl don
10 hydrofolate dehydrogenase (FDH), converts 10-formyltetrahydrofolate (10-formyl-THF) to tetrahydrofola
11 explained by the rapid oxidation of (6S)-10-formyltetrahydrofolate (10-HCO-THF), which is produced b
12 ed in over a 6-fold increase in [(13)C(5)]-5-formyltetrahydrofolate ([(13)C(5)]-5-formylTHF) concentr
13 ligase (5-FCL) catalyzes the conversion of 5-formyltetrahydrofolate (5-CHO-H(4)PteGlu(n)) to 5,10-met
14 hermodynamic parameters for the binding of 5-formyltetrahydrofolate (5-CHO-H4PteGlun) and its polyglu
16 tant L1210 clonal variant in which MTX and 5-formyltetrahydrofolate (5-CHO-THF) influx was markedly d
20 of the tight-binding dimer are occupied by 5-formyltetrahydrofolate (5-formylTHF), whose N5-formyl ca
22 inistered unnatural carbon-6 isomers, (6R)-5-formyltetrahydrofolate (5-HCO-THF) and (6S)-5,10-metheny
24 mide ribonucleotide transformylase (GART; 10-formyltetrahydrofolate:5'-phosphoribosylglycinamide form
25 ured by 5-methyltetrahydrofolate (5MeTHF), 5-formyltetrahydrofolate (5FoTHF), and folic acid concentr
26 ate-mediated one-carbon metabolism (FOCM), 5-formyltetrahydrofolate (5fTHF), a one-carbon substituted
27 ahydrofolate dehydrogenase (FDH) converts 10-formyltetrahydrofolate, a precursor for nucleotide biosy
28 dihydrofolate reductase activity, lowered 10-formyltetrahydrofolate abundance, downregulation of DHFR
30 rms of folates - 5-methyltetrahydrofolate, 5-formyltetrahydrofolate and 10-formyltetrahydrofolate - t
31 e domain that removes a formyl group from 10-formyltetrahydrofolate and a NADP(+)-dependent dehydroge
32 FS) is the only enzyme known to metabolize 5-formyltetrahydrofolate and catalyzes the conversion of 5
33 approximately 50% decrease in the EC50 for 5-formyltetrahydrofolate and folic acid and the MTX IC50 r
35 for (6S)-N5-methyltetrahydrofolate, (6S)-N5-formyltetrahydrofolate and methotrexate compared to the
36 ic production of 5-methyltetrahydrofolate, 5-formyltetrahydrofolate and tetrahydrofolate after 48 h o
37 ormylfolic acid, 5-methyltetrahydrofolate, 5-formyltetrahydrofolate and tetrahydrofolate were determi
38 xymethyltransferase-catalyzed formation of 5-formyltetrahydrofolate, and 5, 10-hydroxymethylenetetrah
39 greater proportions of pteroylmonoglutamate, formyltetrahydrofolate, and 5,10-methenyltetrahyrofolate
40 resulted in augmentation of methotrexate, 5-formyltetrahydrofolate, and 5-methyltetrahydrofolate ini
41 E45K all 1) increased carrier affinity for 5-formyltetrahydrofolate approximately 4-fold, 2) increase
45 nal Rossmann fold domain containing the N-10-formyltetrahydrofolate binding site and a C-terminal sub
48 hile the formyl group is transferred from 10-formyltetrahydrofolate by direct nucleophilic attack by
51 rahydrofolate synthase (MTHFS; also called 5-formyltetrahydrofolate cyclo-ligase; EC 6.3.3.2) activit
64 one of the enzymes of folate metabolism, 10-formyltetrahydrofolate dehydrogenase (FDH), requires a 4
65 the multidomain, multifunctional enzyme, 10-formyltetrahydrofolate dehydrogenase (FDH), using a bacu
69 th alanines resulted in total loss of the 10-formyltetrahydrofolate dehydrogenase activity, whereas t
73 rity between the amino-terminal domain of 10-formyltetrahydrofolate dehydrogenase and methionyl-tRNA-
75 e model have shown a crucial role for the 10-formyltetrahydrofolate dehydrogenase enzyme in serine-to
79 lysis of the product inhibition curve for 10-formyltetrahydrofolate dehydrogenase shows that H4-PteGl
83 ependent crystallographic support in work on formyltetrahydrofolate dehydrogenase, work which further
84 how much of a physiologic dose of [(13)C5]5-formyltetrahydrofolate delivered in a pH-sensitive enter
85 residue N-terminal domain catalyzes the N-10-formyltetrahydrofolate-dependent formylation of the 4''-
86 id to UDP-4-keto-arabinose and (ii) the N-10-formyltetrahydrofolate-dependent formylation of UDP-4-am
87 -pentapyranosyl-4' '-ulose] and (2) the N-10-formyltetrahydrofolate-dependent formylation of UDP-Ara4
88 f [(3)H]5-methyltetrahydrofolate and [(3)H]5-formyltetrahydrofolate (di- through heptaglutamates).
89 transport, subsequent pemetrexed and (6S)-5-formyltetrahydrofolate export into the cytosol was marke
91 in bears a folate binding site, possesses 10-formyltetrahydrofolate hydrolase activity, and exists as
92 ino-terminal domain (residue 1-310) bears 10-formyltetrahydrofolate hydrolase activity, the carboxyl-
93 he Escherichia coli genes purU and purN, N10-formyltetrahydrofolate hydrolase and glycinamide ribonuc
95 enyltetrahydrofolate is hydrolyzed to only 5-formyltetrahydrofolate if reducing agents are present or
96 yl group of serine and the formyl group of 5-formyltetrahydrofolate in complexes of these species wit
99 a likely source of CO(2) production from 10-formyltetrahydrofolate in mitochondria and plays an esse
100 anisms, the addition of p-aminobenzoate or 5-formyltetrahydrofolate in the external medium restored t
101 olysis of 5,10-methenyltetrahydrofolate to 5-formyltetrahydrofolate in vivo, and there is no requirem
102 ce large quantities of folate, and [(13)C5]5-formyltetrahydrofolate infused during colonoscopy is abs
104 drofolate hydrolase uses water to cleave N10-formyltetrahydrofolate into tetrahydrofolate and formate
108 hereas folE thyA mutants supplemented with 5-formyltetrahydrofolate (lacking pterins and depleted in
109 rofolate in mammalian cells, intracellular 5-formyltetrahydrofolate levels were depleted in human 5Y
110 indicated that HypX releases CO using N(10)-formyltetrahydrofolate (N(10)-formyl-THF) as the substra
111 nt in mouse liver and kidney does not bind 5-formyltetrahydrofolate, nor does it oligomerize with the
112 mined the effects of depleting cytoplasmic 5-formyltetrahydrofolate on cellular folate concentrations
113 e N terminus of slr0642) enabled growth on 5-formyltetrahydrofolate or folic acid but not on 5-formyl
115 at results from the binding of glycine and 5-formyltetrahydrofolate polyglutamate, a slow tight-bindi
116 replaced with the more physiological 25 nM 5-formyltetrahydrofolate, R5 cells were 2-fold collaterall
117 nd was purified from the culture medium by 5-formyltetrahydrofolate-Sepharose affinity chromatography
119 wed that the abundance of genes encoding the formyltetrahydrofolate synthetase (fthfs, homoacetogens)
120 nase/methenyltetrahydrofolate cyclohydrolase/formyltetrahydrofolate synthetase (MTHFD1) for an associ
121 nase-methenyltetrahydrofolate cyclohydrolase-formyltetrahydrofolate synthetase (MTHFD1) R653Q, may mo
122 nase-methenyltetrahydrofolate cyclohydrolase-formyltetrahydrofolate synthetase (MTHFD1) rs2236225, in
123 drofolate dehydrogenase, cyclohydrolase, and formyltetrahydrofolate synthetase 1 (MTHFD1), we discove
125 n of the methyl groups from choline requires formyltetrahydrofolate synthetase encoded by fhs in R. p
127 antitative PCR of the functional marker gene formyltetrahydrofolate synthetase showed that its expres
128 hylenetetrahydrofolate dehydrogenase, and 10-formyltetrahydrofolate synthetase were also evaluated.
129 luciferase mRNA binds to the cSHMT.glycine.5-formyltetrahydrofolate ternary complex with an apparent
130 hydrofolate, 5-formyltetrahydrofolate and 10-formyltetrahydrofolate - their stabilities during microw
131 ydrofolate and catalyzes the conversion of 5-formyltetrahydrofolate to 5,10-methenyltetrahydrofolate.
133 lyzes the NADP(+)-dependent conversion of 10-formyltetrahydrofolate to CO(2) and tetrahydrofolate (TH
134 se catalyses the transfer of formyl from N10-formyltetrahydrofolate to GAR to yield formyl-GAR and te
135 that catalyzes the oxidative catabolism of 5-formyltetrahydrofolate to p-aminobenzoylglutamate and a
136 sm highly expressed in liver, metabolizes 10-formyltetrahydrofolate to produce tetrahydrofolate (THF)
138 ion, i.e. NADP(+)-dependent conversion of 10-formyltetrahydrofolate to tetrahydrofolate and CO(2), co
139 actions: the NADP+-dependent oxidation of 10-formyltetrahydrofolate to tetrahydrofolate and CO2 and t
140 mains of FDH and allows the conversion of 10-formyltetrahydrofolate to tetrahydrofolate and CO2.
141 enase reaction resulting in conversion of 10-formyltetrahydrofolate to tetrahydrofolate and CO2.
142 2 and the NADP+-independent hydrolysis of 10-formyltetrahydrofolate to tetrahydrofolate and formate.
143 hydrogenase (FDH) catalyzes conversion of 10-formyltetrahydrofolate to tetrahydrofolate in either a d
144 talyzes transfer of a formyl group from N-10-formyltetrahydrofolate to the 4'-amine of UDP-L-Ara4N.
145 ltetrahydrofolate or folic acid but not on 5-formyltetrahydrofolate triglutamate, demonstrating that
146 e site of ArnA transformylase and other N-10-formyltetrahydrofolate-utilizing enzymes suggests that t
148 olic acid was a much better substrate, and 5-formyltetrahydrofolate was a poorer substrate for transp
150 drofolate, 5'-methyltetrahydrofolate, and 5'-formyltetrahydrofolate were 1250, 400, and 360 pmol/L of
151 degradation in vitro with the exception of 5-formyltetrahydrofolate, which may be a storage form of f
152 folinic acid (also known as leucovorin or 5-formyltetrahydrofolate), whose metabolic function remain