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1 reased activity, but not protein content, of glucose 6-phosphate dehydrogenase.
2 ine does not affect the overall structure of glucose 6-phosphate dehydrogenase.
3 ntapeptide derived from the metabolic enzyme glucose-6-phosphate dehydrogenase.
4 regeneration system and the cytosolic enzyme glucose-6-phosphate dehydrogenase.
5 a role outside of its function in activating glucose-6-phosphate dehydrogenase.
6 ctions based on the molecular model of human glucose-6-phosphate dehydrogenase.
7 sses hexokinase and the rate-limiting enzyme glucose-6-phosphate dehydrogenase.
8 r non-specific glycolytic proteins such as d-glucose-6-phosphate dehydrogenase.
9 red lactate dehydrogenase and heat-denatured glucose-6-phosphate dehydrogenase.
10 aemia, and a mutation of G6PD, which encodes glucose-6-phosphate dehydrogenase.
11 ence of 6-aminonicotinamide, an inhibitor of glucose-6-phosphate dehydrogenase.
12 no significant homology with NADP-dependent glucose-6-phosphate dehydrogenases.
13 extensive similarity to an unusual group of glucose-6-phosphate dehydrogenases.
14 ing for cellular NADPH regenerating enzymes (glucose 6-phosphate dehydrogenase, 6-phosphogluconate de
15 ctivity of pentose phosphate pathway enzymes glucose 6-phosphate dehydrogenase, 6-phosphogluconate de
17 ative pentose phosphate pathway (hexokinase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate de
18 oncomitant inhibition of the parasite enzyme glucose-6-phosphate dehydrogenase-6-phosphogluconolacton
19 In P. falciparum , the bifunctional enzyme glucose-6-phosphate dehydrogenase-6-phosphogluconolacton
20 e (70%), phosphoglucose isomerase (65%), and glucose-6-phosphate dehydrogenase (85%), but not phospho
21 ively, decreased TAL expression up-regulated glucose-6-phosphate dehydrogenase activities and GSH lev
23 8 hrs post-PMA injury with a 40% increase in glucose-6-phosphate dehydrogenase activity and a 32% inc
27 rexpression of TAL resulted in a decrease in glucose 6-phosphate dehydrogenase and 6-phosphogluconate
28 reduced levels of TAL resulted in increased glucose 6-phosphate dehydrogenase and 6-phosphogluconate
29 maximal at 72 hrs with an increase of 98% in glucose-6-phosphate dehydrogenase and 346% in 6-phosphog
32 cell barrier function through suppression of glucose-6-phosphate dehydrogenase and antioxidant defens
33 and inhibiting glycolysis by phosphorylating glucose-6-phosphate dehydrogenase and pyruvate kinase mu
34 enzymes of human red blood cell metabolism: glucose-6-phosphate dehydrogenase and pyruvate kinase.
35 ations involving conversion to N(tz) ADPH by glucose-6-phosphate dehydrogenase and reoxidation to N(t
37 cids; it overlaps the 5' end of zwf (encodes glucose-6-phosphate dehydrogenase) and is followed immed
38 talyzed by 6-phosphogluconate dehydrogenase, glucose 6-phosphate dehydrogenase, and glucose 6-phospha
39 ed elevations in the mRNAs for malic enzyme, glucose-6-phosphate dehydrogenase, and 6-phosphogluconat
40 blood cell polymorphisms (ie, hemoglobin S, glucose-6-phosphate dehydrogenase, and alpha-thalassemia
41 n of branched-chain keto acid dehydrogenase, glucose-6-phosphate dehydrogenase, and amidase in both s
42 three enzymes (catechol-O-methyltransferase, glucose-6-phosphate dehydrogenase, and glyceraldehyde-3-
43 ), oxidative stress (glutathione peroxidase, glucose-6-phosphate-dehydrogenase, and ascorbate peroxid
44 , a plasma membrane (PM) marker; activity of glucose-6-phosphate dehydrogenase, assayed as cytosolic
45 h the construction of the molecular model of glucose-6-phosphate dehydrogenase, based on the structur
46 A1 substantially reduced the inactivation of glucose-6-phosphate dehydrogenase by 4-hydroxy-2-nonenal
47 as exemplified for the reaction catalyzed by glucose-6-phosphate dehydrogenase by comparing the 1-(13
48 eric molecular mass of 33.8kDa while that of glucose-6-phosphate dehydrogenase (D-glucose 6-phosphate
49 vivax malaria treatment in individuals with glucose 6-phosphate dehydrogenase deficiency (G6PDd).
50 of pooled severe malaria data reported that glucose-6-phosphate dehydrogenase deficiency (G6PDd) was
51 uinolines cause dose-dependent haemolysis in glucose-6-phosphate dehydrogenase deficiency (G6PDd).
52 acute haemolytic anaemia in individuals with glucose-6-phosphate dehydrogenase deficiency (G6PDd).
54 re both contraindicated for individuals with glucose-6-phosphate dehydrogenase deficiency and in preg
56 5 mg/kg/d for 14 days) without screening for glucose-6-phosphate dehydrogenase deficiency and were fo
57 on in Israel, we found that individuals with glucose-6-phosphate dehydrogenase deficiency had an incr
58 se, fetal hemoglobin, alpha-thalassemia, and glucose-6-phosphate dehydrogenase deficiency had no effe
59 [95% confidence interval {CI}, 0.52-0.90]), glucose-6-phosphate dehydrogenase deficiency in female c
61 lasmic PICD, the phenotypes of patients with glucose-6-phosphate dehydrogenase deficiency suggest tha
63 lpha-thalassemia, 0.3%; ABO group, 0.3%; and glucose-6-phosphate dehydrogenase deficiency, 0.5%) and
64 tors for neurotoxicity, such as prematurity, glucose-6-phosphate dehydrogenase deficiency, or hypoxia
67 No correlation with sickle cell trait or glucose-6-phosphate-dehydrogenase deficiency was observe
69 rofiles, with increased efficacy and reduced glucose 6-phosphate dehydrogenase-dependent hemotoxicity
70 splantation studies in cats heterozygous for glucose-6-phosphate-dehydrogenase, different estimates o
75 d sex-specific QTL underlying differences in glucose-6-phosphate dehydrogenase enzyme activity betwee
77 ith uncomplicated falciparum malaria, normal glucose-6-phosphate dehydrogenase enzyme levels, and hem
78 either 6PGD or another oxidative PPP enzyme, glucose-6-phosphate dehydrogenase, exhibit non-immune he
79 a substrate for an enzyme, F(420)-dependent glucose-6-phosphate dehydrogenase (Fgd), found in few ba
80 The gene fgd, which codes for F420-dependent glucose-6-phosphate dehydrogenase (FGD), was cloned from
82 most commonly mediated by loss of a specific glucose-6-phosphate dehydrogenase (FGD1) or its deazafla
83 of Asp-177 in the His-Asp catalytic dyad of glucose 6-phosphate dehydrogenase from Leuconostoc mesen
85 A large excess of ALDH3A1 also protected glucose-6-phosphate dehydrogenase from inactivation beca
88 immunofluorescence microscopy has shown that glucose-6-phosphate dehydrogenase (G-6-PDase), the rate-
89 tatus of mitochondrial glutathione (GSH) and glucose 6-phosphate dehydrogenase (G6-PD) was restored b
90 -yl)-2,5-diphenyltetrazolium bromide] (MTT), glucose-6-phosphate dehydrogenase (G6DP), and calcein AM
91 Salmonella typhimurium zwf mutants lacking glucose 6-phosphate dehydrogenase (G6PD) activity have i
94 m embryonic stem cells in which the X-linked glucose 6-phosphate dehydrogenase (G6PD) gene had been t
96 autologous marrow transplantation studies of glucose 6-phosphate dehydrogenase (G6PD) heterozygous fe
97 ession of a thoroughly characterized enzyme: glucose 6-phosphate dehydrogenase (G6PD) in human erythr
100 inactivating ATM or its downstream effector glucose 6-phosphate dehydrogenase (G6PD) sensitizes AML
101 gnment of the amino acid (aa) sequence of 52 glucose 6-phosphate dehydrogenase (G6PD) species from 42
102 0 from the 109 kDa Leuconostoc mesenteroides glucose 6-phosphate dehydrogenase (G6PD) were assigned b
103 capitulated by the knockdown of PPP enzymes, glucose 6-phosphate dehydrogenase (G6PD), or 6-phosphogl
104 is, we mutated the substrate binding site of glucose 6-phosphate dehydrogenase (G6PD), which catalyze
105 ivity at doses low enough to be tolerated by glucose 6-phosphate dehydrogenase (G6PD)-deficient indiv
109 ation and isocitrate dehydrogenase (IDH) and glucose-6-phosphate dehydrogenase (G6PD) activities are
110 100,000 parasites per microliter) and normal glucose-6-phosphate dehydrogenase (G6PD) activity (with
111 a set, there were 1,747 patients with normal glucose-6-phosphate dehydrogenase (G6PD) activity enroll
112 riation in isocitrate dehydrogenase (IDH) or glucose-6-phosphate dehydrogenase (G6PD) activity in a s
119 d on the oxidation of G6P in the presence of glucose-6-phosphate dehydrogenase (G6PD) and nicotinamid
120 -A) down-regulated the protein expression of glucose-6-phosphate dehydrogenase (G6PD) and peroxiredox
122 d expression of the PPP rate-limiting enzyme glucose-6-phosphate dehydrogenase (G6PD) associated with
123 atty acids inhibit the expression of hepatic glucose-6-phosphate dehydrogenase (G6PD) by changes in t
124 reduction of NADPH generation via a block of glucose-6-phosphate dehydrogenase (G6PD) by treatment wi
125 .-) production, suggesting that intranuclear glucose-6-phosphate dehydrogenase (G6PD) can control NOX
126 s study investigates the significance of the glucose-6-phosphate dehydrogenase (G6PD) catalyzed oxida
127 mutations of the housekeeping gene encoding glucose-6-phosphate dehydrogenase (G6PD) cause G6PD defi
128 out dose-dependent haemolysis in people with glucose-6-phosphate dehydrogenase (G6PD) deficiencies ha
129 aemolysis, all patients should be tested for glucose-6-phosphate dehydrogenase (G6PD) deficiency (G6P
131 ), alpha thalassaemia, ABO blood groups, and glucose-6-phosphate dehydrogenase (G6PD) deficiency enco
143 ed the association between immune complexes, glucose-6-phosphate dehydrogenase (G6PD) deficiency, and
144 ug can induce haemolysis in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency, nec
145 cause severe haemolysis in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
146 y of radical cure after testing patients for glucose-6-phosphate dehydrogenase (G6PD) deficiency.
147 omplicated by haemolysis in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
148 bin (Hb) data are limited in Southeast Asian glucose-6-phosphate dehydrogenase (G6PD) deficient (G6PD
149 l malaria risk factors, and we also assessed glucose-6-phosphate dehydrogenase (G6PD) enzyme activity
150 d Thailand and involved patients with normal glucose-6-phosphate dehydrogenase (G6PD) enzyme activity
154 2) IL-1beta stimulated increased activity of glucose-6-phosphate dehydrogenase (G6PD) in a time- and
156 other objective was to determine the role of glucose-6-phosphate dehydrogenase (G6PD) in regulating D
157 s in mitochondria, whereas chloroquine and a glucose-6-phosphate dehydrogenase (G6PD) inhibitor affec
158 We present an overview of small molecule glucose-6-phosphate dehydrogenase (G6PD) inhibitors that
172 hrough microscopy and had normal function of glucose-6-phosphate dehydrogenase (G6PD) on colorimetric
173 , which was exacerbated in erythrocytes from glucose-6-phosphate dehydrogenase (G6PD) patients and re
177 feasibility of point-of-care, quantitative, glucose-6-phosphate dehydrogenase (G6PD) testing followe
179 t of reductive capacity by overexpression of glucose-6-phosphate dehydrogenase (G6PD), a key enzyme f
180 f taxanes, anthracyclines, and inhibitors of glucose-6-phosphate dehydrogenase (G6PD), an enzyme invo
181 levels, which in turn involves modulation of glucose-6-phosphate dehydrogenase (G6PD), an enzyme that
182 y (PPP) is necessary for NET release because glucose-6-phosphate dehydrogenase (G6PD), an important e
183 rised on the haemoglobin subunit beta (HBB), glucose-6-phosphate dehydrogenase (G6PD), atypical chemo
185 ented expression and enzymatic activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione re
186 rum is observed in a population deficient in glucose-6-phosphate dehydrogenase (G6PD), particularly i
187 osphate (NADPH), suppressing the activity of glucose-6-phosphate dehydrogenase (G6PD), resulting in n
188 ene expression of GLUT1 glucose transporter, glucose-6-phosphate dehydrogenase (G6PD), superoxide dis
191 the bacterial pathogen Pseudomonas syringae Glucose-6-phosphate dehydrogenase (G6PD), the key enzyme
193 dinucleotide phosphate (NADPH) at two steps, glucose-6-phosphate dehydrogenase (G6PD), the most commo
197 ose phosphate pathway through the actions of glucose-6-phosphate dehydrogenase (G6PD), the rate-limit
199 the activity of another cytoplasmic enzyme, glucose-6-phosphate dehydrogenase (G6PD), was also measu
200 This expansion is due to up-regulation of glucose-6-phosphate dehydrogenase (G6PD), which stimulat
203 ne deacetylase (HDAC) inhibitors (HDACis) in glucose-6-phosphate dehydrogenase (G6PD)-deficient cells
212 lucose uptake with a concomitant increase in glucose-6-phosphate dehydrogenase (G6PDH) activity, the
213 eveloped by using a coupled enzyme system of glucose-6-phosphate dehydrogenase (G6PDH) and bacterial
214 investigated the reactivation of aggregated glucose-6-phosphate dehydrogenase (G6PDH) by ClpB and it
220 toxification enzymes such as NQO1 as well as glucose-6-phosphate dehydrogenase (G6PDH), a regulator o
221 he Pseudomonas aeruginosa zwf gene, encoding glucose-6-phosphate dehydrogenase (G6PDH), an enzyme tha
222 linked isocitrate dehydrogenase (NADP-ICDH), glucose-6-phosphate dehydrogenase (G6PDH), and, glutathi
223 showed here that a mutation in zwf, encoding glucose-6-phosphate dehydrogenase (G6PDH), leads to a ap
228 xokinase (ATP into glucose 6-phosphate), and glucose 6-phosphate dehydrogenase (glucose 6-phosphate i
229 athione (GSH), glutathione peroxidase (GPX), glucose 6-phosphate dehydrogenase, glutathione reductase
230 ant enzymes including alcohol dehydrogenase, glucose 6-phosphate dehydrogenase, glycerol 3-phosphate
231 ontinuous assay, using glucokinase (Glk) and glucose-6-phosphate dehydrogenase (Gpd) from Thermotoga
234 viously studies using X-linked genes such as glucose-6-phosphate dehydrogenase have been handicapped
235 sis of autologous transplantation studies in glucose-6-phosphate dehydrogenase heterozygous cats to d
237 Here we report point mutations in the human glucose-6-phosphate dehydrogenase (hG6PD) gene transferr
238 The frequencies of low-activity alleles of glucose-6-phosphate dehydrogenase in humans are highly c
239 hibition of the pentose phosphate pathway by glucose-6-phosphate dehydrogenase inhibitors and siRNA s
240 e of the bacterial Leuconostoc mesenteroides glucose-6-phosphate dehydrogenase, it has been possible
241 , mRNAs for several other lipogenic enzymes (glucose-6-phosphate dehydrogenase, malic enzyme, glycero
243 placebo-controlled study, 16 malaria-naive, glucose-6-phosphate dehydrogenase-normal participants ag
244 strate and coenzyme binding and catalysis of glucose-6-phosphate dehydrogenase of Leuconostoc mesente
245 nolysis-derived glucose-1-phosphate enhances glucose-6-phosphate dehydrogenase oligomerization and ac
246 e did not observe changes in the activity of glucose-6-phosphate dehydrogenase or in the pentose phos
247 stroy the tissues to study the haplotypes of glucose-6-phosphate dehydrogenase or to determine the re
250 mmed RA T cells includes glycolytic enzymes (glucose-6-phosphate dehydrogenase, phosphofructokinase),
251 ococcal mutants deficient in PavA, CodY, and glucose-6-phosphate dehydrogenase pointing to the robust
253 ependence of the kinetic parameters of D177N glucose 6-phosphate dehydrogenase results from an ionize
255 eveloped by utilizing a "wired" thermostable glucose-6-phosphate dehydrogenase (tG6PDH) from the hype
256 Mycobacterium smegmatis was found to have a glucose-6-phosphate dehydrogenase that was dependent on
257 ibrosis transmembrane conductance regulator, glucose-6-phosphate dehydrogenase, the neural cell adhes
258 -1 but no changes in glutathione peroxidase, glucose-6-phosphate dehydrogenase, thiols, or catalase.
259 ecific inhibitor (dehydroepiandrosterone) of glucose-6-phosphate dehydrogenase together established r
260 nternal control was shown by comparison with glucose-6-phosphate dehydrogenase transcript levels in 1
262 erase 3, solute carrier family 22 member 16, glucose 6-phosphate dehydrogenase, very long chain fatty
263 The three-dimensional structure of the H240N glucose 6-phosphate dehydrogenase was determined at 2.5
264 smutase 1, glutathione S-transferase-pi, and glucose-6-phosphate dehydrogenase was unaffected by cast
265 peroxidase, NADH/NADP+ transhydrogenase, and glucose-6-phosphate dehydrogenase were most strongly ind
266 of the cytosolic isocitrate dehydrogenase or glucose-6-phosphate dehydrogenase, which also produce cy
267 ersensitivity to SFK2 yielded ZWF1, encoding glucose-6-phosphate dehydrogenase, which has been shown
268 strain over-expressing zwf gene (coding for glucose-6-phosphate dehydrogenase), WX-zwf, produced the
269 own previously to require function of either glucose-6-phosphate dehydrogenase (ZWF1) or cytosolic NA
270 ted an investigation of mutants defective in glucose-6-phosphate dehydrogenase (Zwf1), which catalyze
271 ells grown on glucose has been attributed to glucose-6-phosphate dehydrogenase (Zwf1p) and a cytosoli