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1 ve and accumulates in the nucleus by sensing glucose 6-phosphate.
2 lyzes the phosphorylation of glucose to form glucose 6-phosphate.
3 bHK1 is not subject to inhibition by ADP and glucose 6-phosphate.
4 rythrose 4-phosphate, and with the substrate glucose 6-phosphate.
5 gh the conversion of glucose 1-phosphate and glucose 6-phosphate.
6 Xu5P = xylulose 5-phosphate, G6P = glucose 6-phosphate.
7 agy appears to be regulated by a decrease in glucose-6 phosphate.
8 d growth on minimal medium supplemented with glucose-6-phosphate.
9 nd secondary metabolism via the oxidation of glucose-6-phosphate.
10 concentrations of metabolites, particularly glucose-6-phosphate.
11 xin reductase (TrxR)1 cytoplasmic isoform 3, glucose-6-phosphate 1-dehydrogenase isoform a, Hsp105, v
12 dose reductase, thioredoxin reductase 1, and glucose-6-phosphate 1-dehydrogenase-were identified that
13 GM, Mg(2+)-phospho-beta-PGM, and Mg(2+)-beta-glucose-6-phosphate-1-phosphorane-beta-PGM complexes to
14 it partitions to form glucose 1-phosphate or glucose 6-phosphate 14.3 times more frequently than it d
15 nosamine from glucose-6-phosphate: NtdC is a glucose-6-phosphate 3-dehydrogenase, NtdA is a pyridoxal
16 he half-maximal activation concentration for glucose 6-phosphate (A(0.5)) was increased to 830 +/- 12
18 orresponding to the basal activity state and glucose-6-phosphate activated state of yeast glycogen sy
21 zyme, which catalyses the interconversion of glucose 6-phosphate and fructose 6-phosphate, has been s
24 ficiency were associated with a reduction in glucose 6-phosphate and oleoyl-CoA levels, as well as a
26 have identified dihydroxyacetone phosphate, glucose-6-phosphate and fructose-6-phosphate as addition
29 rylaldehyde-3-phosphate, ribose-5-phosphate, glucose-6-phosphate, and mannose-6-phosphate was achieve
30 mplished using isotopically labeled glucose, glucose-6-phosphate, and pyruvate as internal standards.
31 ase activity due to increased hexokinase II, glucose-6-phosphate, and RGL and PTG levels and enhanced
34 because it catalyses import into plastids of glucose-6-phosphate as the substrate for NADPH generatio
35 eaflet of mitochondria; however, the site of glucose 6-phosphate association responsible for the rele
36 PGI/PMI) has been determined in complex with glucose 6-phosphate at 1.16 A resolution and with fructo
37 esults here implicate a primary role for the glucose 6-phosphate binding site at the N-terminal half
39 S is regulated by allosteric activation upon glucose-6-phosphate binding and inactivation by phosphor
46 strates, including citric acid, formic acid, glucose 6-phosphate, capric acid, gamma-hydroxybutyric a
47 te (T6P) is synthesized from UDP-glucose and glucose-6-phosphate (catalyzed by T6P synthase [TPS]), a
48 e interconversion of glucose 1-phosphate and glucose 6-phosphate, catalyzed by Pseudomonas aeruginosa
49 ssociated with intracellular accumulation of glucose-6-phosphate caused by disruption of glycolytic f
50 have shown that a block in the metabolism of glucose 6-phosphate causes transient growth inhibition a
51 initiate glycolysis by converting glucose to glucose-6-phosphate, contains a strong PAR-binding motif
53 mice impairs allosteric activation of GS by glucose 6-phosphate, decreases hepatic glycogen synthesi
54 tatus of mitochondrial glutathione (GSH) and glucose 6-phosphate dehydrogenase (G6-PD) was restored b
57 inactivating ATM or its downstream effector glucose 6-phosphate dehydrogenase (G6PD) sensitizes AML
60 ant enzymes including alcohol dehydrogenase, glucose 6-phosphate dehydrogenase, glycerol 3-phosphate
61 e (70%), phosphoglucose isomerase (65%), and glucose-6-phosphate dehydrogenase (85%), but not phospho
62 a substrate for an enzyme, F(420)-dependent glucose-6-phosphate dehydrogenase (Fgd), found in few ba
64 most commonly mediated by loss of a specific glucose-6-phosphate dehydrogenase (FGD1) or its deazafla
66 -yl)-2,5-diphenyltetrazolium bromide] (MTT), glucose-6-phosphate dehydrogenase (G6DP), and calcein AM
67 ation and isocitrate dehydrogenase (IDH) and glucose-6-phosphate dehydrogenase (G6PD) activities are
68 riation in isocitrate dehydrogenase (IDH) or glucose-6-phosphate dehydrogenase (G6PD) activity in a s
73 d on the oxidation of G6P in the presence of glucose-6-phosphate dehydrogenase (G6PD) and nicotinamid
74 .-) production, suggesting that intranuclear glucose-6-phosphate dehydrogenase (G6PD) can control NOX
75 out dose-dependent haemolysis in people with glucose-6-phosphate dehydrogenase (G6PD) deficiencies ha
76 ), alpha thalassaemia, ABO blood groups, and glucose-6-phosphate dehydrogenase (G6PD) deficiency enco
83 omplicated by haemolysis in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
84 l malaria risk factors, and we also assessed glucose-6-phosphate dehydrogenase (G6PD) enzyme activity
86 s in mitochondria, whereas chloroquine and a glucose-6-phosphate dehydrogenase (G6PD) inhibitor affec
94 hrough microscopy and had normal function of glucose-6-phosphate dehydrogenase (G6PD) on colorimetric
95 , which was exacerbated in erythrocytes from glucose-6-phosphate dehydrogenase (G6PD) patients and re
99 t of reductive capacity by overexpression of glucose-6-phosphate dehydrogenase (G6PD), a key enzyme f
100 y (PPP) is necessary for NET release because glucose-6-phosphate dehydrogenase (G6PD), an important e
101 ented expression and enzymatic activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione re
102 the bacterial pathogen Pseudomonas syringae Glucose-6-phosphate dehydrogenase (G6PD), the key enzyme
105 the activity of another cytoplasmic enzyme, glucose-6-phosphate dehydrogenase (G6PD), was also measu
106 ne deacetylase (HDAC) inhibitors (HDACis) in glucose-6-phosphate dehydrogenase (G6PD)-deficient cells
108 lucose uptake with a concomitant increase in glucose-6-phosphate dehydrogenase (G6PDH) activity, the
109 investigated the reactivation of aggregated glucose-6-phosphate dehydrogenase (G6PDH) by ClpB and it
111 toxification enzymes such as NQO1 as well as glucose-6-phosphate dehydrogenase (G6PDH), a regulator o
112 linked isocitrate dehydrogenase (NADP-ICDH), glucose-6-phosphate dehydrogenase (G6PDH), and, glutathi
113 showed here that a mutation in zwf, encoding glucose-6-phosphate dehydrogenase (G6PDH), leads to a ap
118 ells grown on glucose has been attributed to glucose-6-phosphate dehydrogenase (Zwf1p) and a cytosoli
122 ations involving conversion to N(tz) ADPH by glucose-6-phosphate dehydrogenase and reoxidation to N(t
124 A1 substantially reduced the inactivation of glucose-6-phosphate dehydrogenase by 4-hydroxy-2-nonenal
125 as exemplified for the reaction catalyzed by glucose-6-phosphate dehydrogenase by comparing the 1-(13
126 acute haemolytic anaemia in individuals with glucose-6-phosphate dehydrogenase deficiency (G6PDd).
128 [95% confidence interval {CI}, 0.52-0.90]), glucose-6-phosphate dehydrogenase deficiency in female c
130 lpha-thalassemia, 0.3%; ABO group, 0.3%; and glucose-6-phosphate dehydrogenase deficiency, 0.5%) and
131 tors for neurotoxicity, such as prematurity, glucose-6-phosphate dehydrogenase deficiency, or hypoxia
134 d sex-specific QTL underlying differences in glucose-6-phosphate dehydrogenase enzyme activity betwee
136 ith uncomplicated falciparum malaria, normal glucose-6-phosphate dehydrogenase enzyme levels, and hem
137 A large excess of ALDH3A1 also protected glucose-6-phosphate dehydrogenase from inactivation beca
138 hibition of the pentose phosphate pathway by glucose-6-phosphate dehydrogenase inhibitors and siRNA s
139 e did not observe changes in the activity of glucose-6-phosphate dehydrogenase or in the pentose phos
140 ococcal mutants deficient in PavA, CodY, and glucose-6-phosphate dehydrogenase pointing to the robust
142 ecific inhibitor (dehydroepiandrosterone) of glucose-6-phosphate dehydrogenase together established r
143 strain over-expressing zwf gene (coding for glucose-6-phosphate dehydrogenase), WX-zwf, produced the
145 blood cell polymorphisms (ie, hemoglobin S, glucose-6-phosphate dehydrogenase, and alpha-thalassemia
146 three enzymes (catechol-O-methyltransferase, glucose-6-phosphate dehydrogenase, and glyceraldehyde-3-
147 either 6PGD or another oxidative PPP enzyme, glucose-6-phosphate dehydrogenase, exhibit non-immune he
148 of the cytosolic isocitrate dehydrogenase or glucose-6-phosphate dehydrogenase, which also produce cy
149 ersensitivity to SFK2 yielded ZWF1, encoding glucose-6-phosphate dehydrogenase, which has been shown
150 In P. falciparum , the bifunctional enzyme glucose-6-phosphate dehydrogenase-6-phosphogluconolacton
151 oncomitant inhibition of the parasite enzyme glucose-6-phosphate dehydrogenase-6-phosphogluconolacton
160 No correlation with sickle cell trait or glucose-6-phosphate-dehydrogenase deficiency was observe
161 xis to induce expression of hexokinase (HK), glucose-6-phosphate dehyrogenase (G6PD) and pyruvate kin
162 osteric activators (fructose-6-phosphate and glucose-6-phosphate) did not always mimic the changes ob
164 the isomerization of fructose-6-phosphate to glucose-6-phosphate (F6P --> G6P) by baker's yeast phosp
165 ic glucose production by failing to redirect glucose-6-phosphate flux from production of glucose to g
166 and mutant hexokinases from mitochondria by glucose 6-phosphate follow equilibrium models, which exp
169 I) and phosphoglucose mutase interconverting glucose 6-phosphate, fructose 6-phosphate, and glucose 1
170 sphate and sedoheptulose 1-phosphate but not glucose 6-phosphate, fructose 6-phosphate, and sedoheptu
172 synthase (mIPS) catalyzes the conversion of glucose-6-phosphate (G-6-P) to inositol-1-phosphate.
173 phosphocreatine (PCr) turnover but increased glucose-6-phosphate (G-6-P) turnover, glucose utilizatio
175 ccomplished by the small molecule effectors, glucose 6-phosphate (G6P) and fructose 1,6-bisphosphate
177 se-6-phosphatase catalyzes the hydrolysis of glucose 6-phosphate (G6P) to glucose and inorganic phosp
178 ion of beta-glucose 1-phosphate (betaG1P) to glucose 6-phosphate (G6P) using Asp8 of the core domain
179 beta-D-glucose 1-phosphate (betaG1P) into D-glucose 6-phosphate (G6P) via sequential phosphoryl tran
180 -d-glucose 1-phosphate (beta-G1P) and beta-d-glucose 6-phosphate (G6P), forming beta-d-glucose 1,6-(b
182 x interplay between the allosteric activator glucose-6-phosphate (G6P) and reversible phosphorylation
184 acterium tuberculosis (Mtb) PYK uses AMP and glucose-6-phosphate (G6P) as synergistic allosteric acti
187 se-beta (G6Pase-beta or G6PC3) that converts glucose-6-phosphate (G6P) into glucose, the primary ener
188 gluconeogenesis and glycogenolysis, in which glucose-6-phosphate (G6P) is hydrolyzed to glucose for r
191 a like Escherichia coli, the accumulation of glucose-6-phosphate (G6P) or its analogs such as alpha-m
192 d previously that increased carbon flux from glucose-6-phosphate (G6P) through the pentose phosphate
193 se-6-phosphatase catalyzes the hydrolysis of glucose-6-phosphate (G6P) to glucose and inorganic phosp
195 Ib (GSD-Ib) is caused by deficiencies in the glucose-6-phosphate (G6P) transporter (G6PT) that have b
196 Ib (GSD-Ib) is caused by a deficiency in the glucose-6-phosphate (G6P) transporter (G6PT) that works
200 t (Arg582Ala) that could not be activated by glucose-6-phosphate (G6P), but possessed full catalytic
201 e (2-DG), iodoacetate (IAA)), intermediates (glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), f
202 in secretion (GSIS) that acts by hydrolyzing glucose-6-phosphate (G6P), thereby reducing glycolytic f
203 se enzymes catalyze conversion of glucose to glucose-6-phosphate (G6P), which is the first step in th
204 ine, fructose, glucose, glucose-1-phosphate, glucose-6-phosphate, galactose, lactose, and sucrose--at
205 e kinase that is allosterically activated by glucose 6-phosphate (Glc-6-P) and adenosine monophosphat
207 final steps of glycogenolysis, intracellular glucose 6-phosphate (Glc-6-P) is transported into the en
208 and isomerization for the interconversion of glucose 6-phosphate (Glc-6-P) to fructose 6-phosphate (F
209 e allosteric inhibition of E. coli FBPase by glucose 6-phosphate (Glc-6-P), the first metabolite prod
210 generated between meals by the hydrolysis of glucose-6-phosphate (Glc-6-P) in the liver and the kidne
211 nd with the cofactor GlcN6P or the inhibitor glucose 6-phosphate (Glc6P) at 1.7 A and 2.2 A resolutio
212 me bound to a naturally occurring inhibitor, glucose 6-phosphate (Glc6P), and a nonnatural activating
213 tdA is a pyridoxal phosphate-dependent 3-oxo-glucose-6-phosphate:glutamate aminotransferase, and NtdB
214 were responsible for generating two NADH per glucose-6-phosphate (i.e., four electrons were generated
215 ehyde-3-phosphate, fructose-6-phosphate, and glucose-6-phosphate; (ii) has smaller cells (diameter ca
217 k that was stripped of intrinsic glucose and glucose 6-phosphate in order to obtain standards and sam
218 tes glucose homeostasis, converts glucose to glucose-6-phosphate in pancreatic beta-cells, liver hepa
221 the structure of mIPS with a trapped 5-keto-glucose-6-phosphate intermediate at 2 A resolution by a
222 combination with conversion of the formed d-glucose-6-phosphate into mixtures of labeled methyl d-gl
223 poptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway t
224 T2 expression by Suc increases the import of glucose-6-phosphate into the plastids that would repress
225 zyme-catalyzed phosphorylation of glucose to glucose-6-phosphate is a reaction central to the metabol
226 we demonstrate that the enzyme's response to glucose-6-phosphate is controlled by Arg583 and Arg587,
228 6.TCR.Calpha(-/-)H-2(b/g7) mice induced anti-glucose 6-phosphate isomerase antibody-dependent chronic
229 y passive transfer of autoantibodies against glucose 6-phosphate isomerase is transient and therefore
230 elping B cells to produce arthritogenic anti-glucose-6-phosphate isomerase (anti-GPI) autoantibodies.
231 atoid arthritis, autoantibodies specific for glucose-6-phosphate isomerase (GPI) can transfer joint-s
233 ceptors (BCRs) with different affinities for glucose-6-phosphate isomerase (GPI) were examined in the
234 vealed a point mutation, Gly-189 --> Glu, in glucose-6-phosphate isomerase (GPI), a glycolytic enzyme
235 high titers of antibodies against the enzyme glucose-6-phosphate isomerase (GPI), promoted by CD4(+)
236 autoimmune arthritis by tracking the fate of glucose-6-phosphate isomerase (GPI)-reactive CD4(+) T ce
238 thal phenotype of RNAi-mediated depletion of glucose-6-phosphate isomerase (PGI) in the glucose-deple
241 se and reduced deposition of pathogenic anti-glucose-6-phosphate isomerase Abs in the joint (with a r
243 inefficient at taking up the key autoantigen glucose-6-phosphate isomerase and that Msr1-deficient mi
244 uld not be reproduced by increasing the anti-glucose-6-phosphate isomerase antibody load, which demon
245 mber of the IL-1 family, can exacerbate anti-glucose-6-phosphate isomerase autoantibody-induced arthr
246 e model of arthritis, autoantibodies against glucose-6-phosphate isomerase cause joint-specific infla
247 osure, twice-a-day treatment with 17l in the glucose-6-phosphate isomerase chronic in vivo mouse mode
248 (2) died in galactose medium as well as when glucose-6-phosphate isomerase was knocked down, suggesti
249 to [6,6'-(3)H]Fru-2,6-P(2) using hexokinase, glucose-6-phosphate isomerase, and 6-phosphofructo-2-kin
250 ormation and autoantibody production against glucose-6-phosphate isomerase, leading to joint inflamma
251 e in the titer of serum antibodies targeting glucose-6-phosphate isomerase, the relevant autoantigen,
252 ransgenic mice specific for the self-antigen glucose-6-phosphate isomerase, we show that autoreactive
253 icro-positron emission tomography that these glucose-6-phosphate isomerase-specific autoantibodies ra
257 .5 +/- 0.5 %ID/g), as early as 1 d after the glucose-6-phosphate-isomerase serum injection, a time po
259 nalogous to the Entner-Doudoroff pathway for glucose-6-phosphate: It involves an NAD(+)-dependent SQ
260 tes, this regulation is accomplished through glucose-6-phosphate levels and protein phosphorylation.
261 patic glucose production and reduces hepatic glucose-6-phosphate levels to complete a homeostatic loo
263 -> UDP-glucose <--> glucose 1-phosphate <--> glucose 6-phosphate <--> fructose 6-phosphate, showed a
265 pathway suggests that in addition to sensing glucose 6-phosphate, MondoA can also sense glucosamine 6
266 catalyze the biosynthesis of kanosamine from glucose-6-phosphate: NtdC is a glucose-6-phosphate 3-deh
267 sitol is generated by de novo synthesis from glucose 6-phosphate or is provided from the environment
271 ADP-dependent glucokinase (ADPGK) catalyzes glucose-6-phosphate production, utilizing ADP as a phosp
274 ing isolated intact liver or fat microsomes, glucose-6 phosphate stimulated 11 beta-HSD1 oxo-reductas
275 n storage phenotype by genetic inhibition of glucose-6-phosphate-stimulated glycogen synthase activit
276 lator of basal GSIS that acts by hydrolyzing glucose-6-phosphate, thereby reducing glycolytic flux.
277 P-glucuronate) stemmed from UDP-glucose, not glucose 6-phosphate; therefore, UDP-glucuronate arose pr
278 The encoded 62-kDa human enzyme converted d-glucose 6-phosphate to 1-d-myo-inositol 3-phosphate, the
279 he de novo synthesis is the isomerization of glucose 6-phosphate to 1-D-myo-inositol-3-phosphate, cat
280 t equatorial transamination of 3-oxo-alpha-D-glucose 6-phosphate to form alpha-D-kanosamine 6-phospha
282 G-6-Pase) catalyzes the dephosphorylation of glucose-6-phosphate to glucose, an opposite process to g
287 ense oligonucleotides (ASOs) specific to the glucose 6-phosphate transporter-1 (G6PT1) enabled reduct
288 e disease type-Ib (GSD-Ib), deficient in the glucose-6-phosphate transporter (G6PT), is characterized
290 tid, on the one hand, and up-regulation of a GLUCOSE-6-PHOSPHATE TRANSPORTER (GPT2), on the other han
291 omal-recessive disease caused by mutation of glucose-6-phosphate transporter and characterized by alt
292 this question, we investigated the effect of glucose-6-phosphate transporter mutation on immune cell
293 gh the study of neutrophils deficient in the glucose-6-phosphate transporter, describe a novel role f
294 olyphosphate glucokinase converts glucose to glucose-6-phosphate using low-cost, stable polyphosphate
296 e values of K(m) for glucose-1-phosphate and glucose-6-phosphate were determined using the substrate-
297 it interface is rearranged by the binding of glucose-6-phosphate, which frees the active site cleft a
298 supplementation of Xenopus egg extract with glucose-6-phosphate, which promotes caspase-2/14-3-3zeta
299 ion, glucose 1,6-bisphosphate is formed from glucose 6-phosphate with a rate constant of 12 s(-)(1),
300 iauxic growth on glucose/lactose and glucose/glucose-6-phosphate with that of the individual models.
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