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1  in the form of 5,10-ethenyl-tetrahydrofolyl polyglutamate.
2 H]compound 1 was metabolized to (3)H-labeled polyglutamates.
3 yglutamyl tail from folyl and p-aminobenzoyl polyglutamates.
4 TX accumulation and metabolism to long-chain polyglutamates.
5  rotate, was rapidly converted to long-chain polyglutamates.
6  the gamma-linked glutamates from folic acid polyglutamates.
7 d penultimate gamma-linkages of methotrexate polyglutamates.
8 rom HL-60 cells were similar on methotrexate polyglutamates.
9                                              Polyglutamate, a peptide reported to mitigate aluminum t
10 ding of glycine and 5-formyltetrahydrofolate polyglutamate, a slow tight-binding inhibitor.
11  metabolically trapped in mammalian cells as polyglutamates, a process catalyzed by folylpoly-gamma-g
12 i) folates continuously enter the vacuole as polyglutamates, accumulate there, are hydrolyzed by GGH,
13                            Whereas C1 and C2 polyglutamates accumulated to similar levels in WT and R
14 basis for differences between long chain MTX polyglutamate accumulation between different leukemia ce
15          We now report that LY231514 and its polyglutamates also markedly inhibit other key folate-re
16 t study, we measured intracellular levels of polyglutamated anabolites of 1031U89, 1843U89, and three
17          Each TS inhibitor was anabolized to polyglutamated analogues with one to five added glutamyl
18 ound is as potent an enzyme inhibitor as its polyglutamated analogues.
19                           Polyanions such as polyglutamate and double-stranded and single-stranded DN
20  resembles the Raman amide I band of ionized polyglutamate and polylysine, peptides which adopt a pol
21 ication were 1.6 and 5 nmol/L for individual polyglutamates and 1.5 and 4.5 nmol/L for total polyglut
22  was contributed by 5-methyltetrahydrofolate polyglutamates and 5,10-methenyltetrahydrofolate polyglu
23 s caused extensive deglutamylation of folate polyglutamates and lowered the total folate content by a
24 ts transport characteristics with respect to polyglutamates and reduced folates are not identical to
25 en leukemia cells that accumulate long chain polyglutamates and those that do not were differences in
26 y this route was rapidly converted to higher polyglutamates and, when grown with 25 nM 5-formyl-tetra
27  selectivity of the transporter for MTX, MTX polyglutamates, and physiological folates.
28 selectivity of this transporter for MTX, MTX polyglutamates, and physiological folates.
29 itochondrial FPGS is required because folate polyglutamates are not substrates for transport across t
30 lpolyglutamates in vacuoles implies that the polyglutamates are somehow protected from GGH attack.
31 to SHMT, showing that anions compete for the polyglutamate binding site.
32                       Both polyaspartate and polyglutamate blocked LPL and chylomicron binding to GPI
33 showed approximately 85% reduction in folate polyglutamates, but cells expressing LeGGH3 did not, con
34 the biosynthesis of F(420)-0 (F(420) without polyglutamate), by transferring the lactyl phosphate moi
35  DNA-like polyanion chains (e.g. heparin and polyglutamate) can mediate the transfer.
36 retention (associated with tissue storage of polyglutamates) can contribute to clinical toxicities, 1
37 rmidis contains the cap operon, encoding the polyglutamate capsule, a major virulence factor in Bacil
38 lthough transport gradually decreased as the polyglutamate chain length increased, both MTX-Glu(2) an
39 cid concentrations, and 4) increased average polyglutamate chain lengths of folate cofactors.
40  katanin hexamer central pore constrains the polyglutamate chain patterns on beta-tails recognized pr
41                                          The polyglutamate chain, which does not contribute to cataly
42      HDMTX plus MP yielded 2-fold higher MTX polyglutamate concentrations than LDMTX plus MP (2148 +/
43  for neuronal survival through hydrolysis of polyglutamate-containing substrates.
44  by a 2-fold increase in accumulation of MTX polyglutamate derivatives and a approximately 50% decrea
45 ct to steady state kinetics, chain length of polyglutamate derivatives formed, and end-product inhibi
46             The excess folate accumulated as polyglutamate derivatives in the vacuole.
47 enous folate pools were modestly reduced but polyglutamate derivatives of DDATHF and ALIMTA (LY231514
48 oform was also capable of forming long chain polyglutamate derivatives of the model folate, 5,10-dide
49     The biosynthetic pathway converts GTP to polyglutamated derivatives of tetrahydrofolate (THF), es
50  of thioguanine nucleotides and methotrexate polyglutamates did not differ between the 4 BMI groups (
51 , there was no detectable transfer of folate polyglutamates either from the cytosol to mitochondria,
52 l glutamates to folate, forming gamma-linked polyglutamate folates of varying lengths.
53  these parasites could still convert pABA to polyglutamated folates, albeit at a very low level, but
54 al pteroylmonoglutamate was converted to the polyglutamate form, most of the body folate was visceral
55 ndogenously, folates exist in the brain in a polyglutamated form with 1-7 terminal glutamates (approx
56 talyze sequential reactions in coenzyme F420 polyglutamate formation: a gamma-glutamyl ligase adds 1-
57 ubstrate are tight-binding ligands, and that polyglutamate forms enhance the affinity of both substra
58       Metabolism to more biologically active polyglutamate forms is also potentiated for MTX and othe
59 ethod does not distinguish between mono- and polyglutamate forms of the coenzyme.
60 w Kms for folylpolyglutamate synthetase, and polyglutamate forms of these inhibitors are accumulated
61 yltetrahydrofolate (5-CHO-H4PteGlun) and its polyglutamate forms to rabbit liver cytosolic serine hyd
62 lished that LY231514 and its synthetic gamma-polyglutamates (glu3 and glu5) exert potent inhibition a
63  the presence of formylated tetrahydrofolate polyglutamates in addition to methylated derivatives in
64 method for the determination of methotrexate polyglutamates in dried blood spots (DBS).
65 n mechanism of self-assembly for star-shaped polyglutamates in nonsalty aqueous solutions is identifi
66 onomers, and to contain tightly bound folate polyglutamates in vivo.
67 mylation, augmented hydrolysis of antifolate polyglutamates, increased expression and mutation of tar
68 f these nanosized soft-assembled star-shaped polyglutamates is also described, enabling the translati
69 rates and a marked preference for long-chain polyglutamates (Km values for glu4 versus glu1 derivativ
70 similarities were present in the folyl-gamma-polyglutamate ligases.
71 several key folate-requiring enzymes via its polyglutamated metabolites.
72 sting cofactor 5,10-methenyl-tetrahydrofolyl-polyglutamate (MTHF) and the catalytic cofactor flavin a
73 nt, which is a 5,10-methenyltetrahydrofolate polyglutamate (MTHF) in most cases.
74 here was a significant decrease in the total polyglutamated MTX in the gut in the GLN group.
75                              Erythrocyte MTX-polyglutamates (MTX-PG(1-5)) may be used for therapeutic
76 the mechanism for higher accumulation of MTX polyglutamates (MTX-PG) in hyperdiploid ALL and lower ac
77             Intracellular methotrexate (MTX) polyglutamates (MTXGlu) have been shown to be potentiall
78  assessed by measuring concentrations of MTX polyglutamates (MTXGlu), has been demonstrated to be a p
79              To determine whether higher MTX polyglutamate (MTXPG) concentrations in ALL blasts trans
80 of leukemia cells to accumulate methotrexate polyglutamate (MTXPG) is an important determinant of the
81 ith significantly higher accumulation of MTX polyglutamates (MTXPG(4-7)) in ALL cells.
82 ular metabolism of methotrexate (MTX) to MTX-polyglutamates (MTXPG) is one determinant of cytotoxicit
83 f its effects through polyglutamation to MTX polyglutamates (MTXPGs) and inhibition of 5-aminoimidazo
84 od cell (RBC) concentrations of methotrexate polyglutamates (MTXPGs) and thioguanine nucleotides (TGN
85                                 Methotrexate polyglutamates (MTXPGs) determine in vivo efficacy in ac
86        Cellular accumulation of methotrexate polyglutamates (MTXPGs) is recognized as an important de
87                 Soy-based formulas contained polyglutamates of 5-formyl-tetrahydrofolate.
88 he bacterial synthesis yielded predominantly polyglutamates of [(3)H]5-methyltetrahydrofolate and [(3
89 ximal gamma-glutamyl linkage of longer chain polyglutamates of folates and their analogues.
90 c leukemia blasts accumulate less long chain polyglutamates of methotrexate (MTX) than acute lymphocy
91 se (GGH) catalyzes degradation of the active polyglutamates of natural folates and the antifolate met
92              The effects of LY231514 and its polyglutamates on aminoimidazole carboxamide ribonucleot
93 osophila melanogaster spastin hexamer with a polyglutamate peptide bound in its central pore.
94 n, we tested the ability of polyaspartate or polyglutamate peptides to block the binding of ligands t
95 lic acid exposure was in the form of dietary polyglutamates rather than the more easily absorbed supp
96 yglutamates and 1.5 and 4.5 nmol/L for total polyglutamates, respectively.
97  5-formyl- and 5,10-methenyltetrahydrofolate polyglutamates, respectively.
98 n of thioguanine nucleotides or methotrexate polyglutamates, respectively.
99 cognises and removes glutamate residues from polyglutamated RpsF and stimulates poly-alpha-L-glutamat
100                                          The polyglutamate serves therefore an additional function as
101 rboxypeptidase (CCP) family that metabolizes polyglutamate side chain and its loss results in neurode
102 re of Fhc to investigate the function of the polyglutamate side chain in MYFR and the relatedness of
103         This negatively charged and branched polyglutamate side chain interacts with a cluster of con
104  of Fhc together with MYFR revealed that the polyglutamate side chain of MYFR is branched and contain
105 torquens, MYFR contains a large and branched polyglutamate side chain of up to 24 glutamates.
106  extorquens and identified an unusually long polyglutamate side chain of up to 24 glutamates.
107 mylation, where they catalyze the removal of polyglutamate side chains.
108 rrier but, unlike 1, is independent of folyl polyglutamate synthase (FPGS) expression levels and poly
109 , including folate hydrolase (FOLH1), folate polyglutamate synthase (FPGS), gamma-glutamyl hydrolase
110 ells, respectively, because of decreased MTX polyglutamate synthesis (despite having similar levels o
111 ing a mechanism for the regulation of folate polyglutamate synthesis in cells.
112 ediated in vivo by the cellular enzyme folyl polyglutamate synthetase.
113 e cytoplasmic SHMT (cSHMT), lacking only the polyglutamate tail of the inhibitor, has been determined
114 olism and are predominantly decorated with a polyglutamate tail that enhances co-enzyme affinity, sub
115 sidues that contribute to the binding of the polyglutamate tail.
116 brain microtubules is suspected to occur via polyglutamates that are added post-translationally to tu
117  that 3 and its B-ring analogues cannot form polyglutamates, their high cytotoxicity relative to the
118  in regard to i) digestion of dietary folate polyglutamates to folate monoglutamates by the cloning o
119                 The relative contribution of polyglutamates to the total folate content remained low
120  data demonstrate that BCRP is a MTX and MTX-polyglutamate transporter and reveal a possible mechanis
121                     5-Methyltetrahydrofolate polyglutamates were the only folate form found in RBCs f
122 glutamates and 5,10-methenyltetrahydrofolate polyglutamates, which were also major forms of folate in
123    In this study, we examined the ability of polyglutamates with different side-chain moieties-poly-g
124 e cytosol and mitochondria, folates exist as polyglutamates, with polyglutamylation catalyzed by foly

 
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