ライフサイエンスコーパス: glucose-6-phosphate

1 able bacterial PK structure containing bound glucose 6-phosphate).

2 Xu5P = xylulose 5-phosphate, G6P = glucose 6-phosphate.

3 ve and accumulates in the nucleus by sensing glucose 6-phosphate.

4 lyzes the phosphorylation of glucose to form glucose 6-phosphate.

5 bHK1 is not subject to inhibition by ADP and glucose 6-phosphate.

6 gh the conversion of glucose 1-phosphate and glucose 6-phosphate.

7 agy appears to be regulated by a decrease in glucose-6 phosphate.

8 nd secondary metabolism via the oxidation of glucose-6-phosphate.

9 d growth on minimal medium supplemented with glucose-6-phosphate.

10 xin reductase (TrxR)1 cytoplasmic isoform 3, glucose-6-phosphate 1-dehydrogenase isoform a, Hsp105, v

11 nosamine from glucose-6-phosphate: NtdC is a glucose-6-phosphate 3-dehydrogenase, NtdA is a pyridoxal

12 CcpA binding was enhanced upon addition of glucose-6-phosphate, a putative cofactor for CcpA.

13 orresponding to the basal activity state and glucose-6-phosphate activated state of yeast glycogen sy

14 d the incoming glucose producing the product glucose-6-phosphate, also at an elevated rate.

15 plays potent K-type allosteric activation by glucose 6-phosphate and by intermediates from the pentos

16 zyme, which catalyses the interconversion of glucose 6-phosphate and fructose 6-phosphate, has been s

17 alpha-D-glucopyranoside 6-phosphate to yield glucose 6-phosphate and methanol.

18 ficiency were associated with a reduction in glucose 6-phosphate and oleoyl-CoA levels, as well as a

19 hate (1,5AG6P), a close structural analog of glucose-6-phosphate and an inhibitor of low-K (M) hexoki

20 6-P-F-Asp (via an enaminol intermediate) to glucose-6-phosphate and aspartate.

21 have identified dihydroxyacetone phosphate, glucose-6-phosphate and fructose-6-phosphate as addition

22 glycerate and 3-phosphoglycerate, as well as glucose-6-phosphate and fructose-6-phosphate.

23 ganded or bound to the competitive inhibitor glucose-6-phosphate and in the postcleavage state.

24 yrophosphate into ATP), hexokinase (ATP into glucose 6-phosphate), and glucose 6-phosphate dehydrogen

25 cose in the presence of close analogs (i.e., glucose-6-phosphate), and can detect glucose above a thr

26 als-phosphorylates I(3)P(1) originating from glucose-6-phosphate, and I(1)P(1) generated from sphingo

27 rylaldehyde-3-phosphate, ribose-5-phosphate, glucose-6-phosphate, and mannose-6-phosphate was achieve

28 mplished using isotopically labeled glucose, glucose-6-phosphate, and pyruvate as internal standards.

29 ase activity due to increased hexokinase II, glucose-6-phosphate, and RGL and PTG levels and enhanced

30 d-Glucose and d-glucose-6-phosphate are direct agonists of both LXR-alph

31 EBs preferentially used glucose-6-phosphate as an energy source, whereas RBs req

32 because it catalyses import into plastids of glucose-6-phosphate as the substrate for NADPH generatio

33 We propose a mechanism by which glucose 6-phosphate binding at the allosteric site commu

34 esults here implicate a primary role for the glucose 6-phosphate binding site at the N-terminal half

35 In contrast, mutations that block glucose 6-phosphate binding to the N-terminal half requi

36 S is regulated by allosteric activation upon glucose-6-phosphate binding and inactivation by phosphor

37 on and activated by protein phosphatases and glucose-6-phosphate binding.

38 ykA at 2.4 angstrom resolution revealed that glucose 6-phosphate binds in a pocket that is distinct f

39 Finally, in addition to cyclic glucose 6-phosphate bound at the active site, the hexame

40 rmeable for glucose, glucose 1-phosphate and glucose 6-phosphate, but not for maltose.

41 -d-glucopyranose), which can be converted to glucose 6-phosphate by levoglucosan kinase (LGK).

42 It is synthesized from glucose 6-phosphate by myo-inositol-3-phosphate synthase

43 molecules closely related to GlcN6P, such as glucose-6-phosphate, cannot activate self-cleavage.

44 te (T6P) is synthesized from UDP-glucose and glucose-6-phosphate (catalyzed by T6P synthase [TPS]), a

45 ssociated with intracellular accumulation of glucose-6-phosphate caused by disruption of glycolytic f

46 initiate glycolysis by converting glucose to glucose-6-phosphate, contains a strong PAR-binding motif

47 After UNSAT, but not CHO, muscle glucose-6-phosphate content was 103% higher compared wit

48 mice impairs allosteric activation of GS by glucose 6-phosphate, decreases hepatic glycogen synthesi

49 tatus of mitochondrial glutathione (GSH) and glucose 6-phosphate dehydrogenase (G6-PD) was restored b

50 Individuals with glucose 6-phosphate dehydrogenase (G6PD) deficiency are

51 Glucose 6-phosphate dehydrogenase (G6PD) deficiency is 1

52 Glucose 6-phosphate dehydrogenase (G6PD) is the most com

53 inactivating ATM or its downstream effector glucose 6-phosphate dehydrogenase (G6PD) sensitizes AML

54 , HDACi selectively enhance transcription of glucose 6-phosphate dehydrogenase (G6PD).

55 eductant, NADPH by impairing the activity of glucose 6-phosphate dehydrogenase (G6PD).

56 Moreover, higher activities of glucose 6-phosphate dehydrogenase (G6PDH), 6-phosphogluc

57 xokinase (ATP into glucose 6-phosphate), and glucose 6-phosphate dehydrogenase (glucose 6-phosphate i

58 ant enzymes including alcohol dehydrogenase, glucose 6-phosphate dehydrogenase, glycerol 3-phosphate

59 a substrate for an enzyme, F(420)-dependent glucose-6-phosphate dehydrogenase (Fgd), found in few ba

60 ide transfer coenzyme for an F(420)-specific glucose-6-phosphate dehydrogenase (Fgd).

61 most commonly mediated by loss of a specific glucose-6-phosphate dehydrogenase (FGD1) or its deazafla

62 -yl)-2,5-diphenyltetrazolium bromide] (MTT), glucose-6-phosphate dehydrogenase (G6DP), and calcein AM

63 100,000 parasites per microliter) and normal glucose-6-phosphate dehydrogenase (G6PD) activity (with

64 riation in isocitrate dehydrogenase (IDH) or glucose-6-phosphate dehydrogenase (G6PD) activity in a s

65 Glucose-6-phosphate dehydrogenase (G6PD) activity is ess

66 ATM activation induces glucose-6-phosphate dehydrogenase (G6PD) activity, the l

67 Unexpectedly, Glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogl

68 d on the oxidation of G6P in the presence of glucose-6-phosphate dehydrogenase (G6PD) and nicotinamid

69 -A) down-regulated the protein expression of glucose-6-phosphate dehydrogenase (G6PD) and peroxiredox

70 Patients (aged >=6 months) with normal glucose-6-phosphate dehydrogenase (G6PD) and presenting

71 .-) production, suggesting that intranuclear glucose-6-phosphate dehydrogenase (G6PD) can control NOX

72 out dose-dependent haemolysis in people with glucose-6-phosphate dehydrogenase (G6PD) deficiencies ha

73 aemolysis, all patients should be tested for glucose-6-phosphate dehydrogenase (G6PD) deficiency (G6P

74 ), alpha thalassaemia, ABO blood groups, and glucose-6-phosphate dehydrogenase (G6PD) deficiency enco

75 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a

76 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is b

77 The global prevalence of X-linked glucose-6-phosphate dehydrogenase (G6PD) deficiency is t

78 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is t

79 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is t

80 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is t

81 Despite glucose-6-phosphate dehydrogenase (G6PD) deficiency prev

82 ug can induce haemolysis in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency, nec

83 omplicated by haemolysis in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency.

84 bin (Hb) data are limited in Southeast Asian glucose-6-phosphate dehydrogenase (G6PD) deficient (G6PD

85 d Thailand and involved patients with normal glucose-6-phosphate dehydrogenase (G6PD) enzyme activity

86 l malaria risk factors, and we also assessed glucose-6-phosphate dehydrogenase (G6PD) enzyme activity

87 The inhibition of glucose-6-phosphate dehydrogenase (G6PD) expression by a

88 s in mitochondria, whereas chloroquine and a glucose-6-phosphate dehydrogenase (G6PD) inhibitor affec

89 Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme

90 The enzyme glucose-6-phosphate dehydrogenase (G6PD) is a major cont

91 Glucose-6-phosphate dehydrogenase (G6PD) is critical in

92 The gene coding for glucose-6-phosphate dehydrogenase (G6PD) is subject to p

93 The reaction catalyzed by glucose-6-phosphate dehydrogenase (G6PD) is the first, r

94 Glucose-6-phosphate dehydrogenase (G6PD) is the principa

95 Glucose-6-phosphate dehydrogenase (G6PD) is the rate-lim

96 Glucose-6-phosphate dehydrogenase (G6PD) modulates vascu

97 hrough microscopy and had normal function of glucose-6-phosphate dehydrogenase (G6PD) on colorimetric

98 , which was exacerbated in erythrocytes from glucose-6-phosphate dehydrogenase (G6PD) patients and re

99 Glucose-6-phosphate dehydrogenase (G6PD) regulates produ

100 Glucose-6-phosphate dehydrogenase (G6PD) status was dete

101 In vivo, pharmacological inhibition of glucose-6-phosphate dehydrogenase (G6PD) to decrease NAD

102 t of reductive capacity by overexpression of glucose-6-phosphate dehydrogenase (G6PD), a key enzyme f

103 f taxanes, anthracyclines, and inhibitors of glucose-6-phosphate dehydrogenase (G6PD), an enzyme invo

104 y (PPP) is necessary for NET release because glucose-6-phosphate dehydrogenase (G6PD), an important e

105 ented expression and enzymatic activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione re

106 However, we found that knockdown of glucose-6-phosphate dehydrogenase (G6PD), the first oxiP

107 the bacterial pathogen Pseudomonas syringae Glucose-6-phosphate dehydrogenase (G6PD), the key enzyme

108 Here we show that glucose-6-phosphate dehydrogenase (G6PD), the rate-limit

109 the activity of another cytoplasmic enzyme, glucose-6-phosphate dehydrogenase (G6PD), was also measu

110 ne deacetylase (HDAC) inhibitors (HDACis) in glucose-6-phosphate dehydrogenase (G6PD)-deficient cells

111 ility is protection from oxidative stress by glucose-6-phosphate dehydrogenase (G6PD).

112 haemolysis in patients with a deficiency in glucose-6-phosphate dehydrogenase (G6PDd).

113 lucose uptake with a concomitant increase in glucose-6-phosphate dehydrogenase (G6PDH) activity, the

114 investigated the reactivation of aggregated glucose-6-phosphate dehydrogenase (G6PDH) by ClpB and it

115 Glucose-6-phosphate dehydrogenase (G6PDH) has been impli

116 toxification enzymes such as NQO1 as well as glucose-6-phosphate dehydrogenase (G6PDH), a regulator o

117 linked isocitrate dehydrogenase (NADP-ICDH), glucose-6-phosphate dehydrogenase (G6PDH), and, glutathi

118 We studied the contribution of glucose-6-phosphate dehydrogenase (Glc-6-PD), an importa

119 compounds that inhibit Plasmodium falciparum glucose-6-phosphate dehydrogenase (PfG6PD).

120 ells grown on glucose has been attributed to glucose-6-phosphate dehydrogenase (Zwf1p) and a cytosoli

121 Also glucose-6-phosphate dehydrogenase activity and NADPH lev

122 nal requirement mediating selection for high glucose-6-phosphate dehydrogenase activity.

123 Two NAD-dependent dehydrogenases (glucose-6-phosphate dehydrogenase and 6-phosphogluconate

124 cal NADPH homeostasis, which is regulated by glucose-6-phosphate dehydrogenase and AMP kinase.

125 cell barrier function through suppression of glucose-6-phosphate dehydrogenase and antioxidant defens

126 ations involving conversion to N(tz) ADPH by glucose-6-phosphate dehydrogenase and reoxidation to N(t

127 Evaluations for glucose-6-phosphate dehydrogenase and thiopurine S-methy

128 A1 substantially reduced the inactivation of glucose-6-phosphate dehydrogenase by 4-hydroxy-2-nonenal

129 as exemplified for the reaction catalyzed by glucose-6-phosphate dehydrogenase by comparing the 1-(13

130 of pooled severe malaria data reported that glucose-6-phosphate dehydrogenase deficiency (G6PDd) was

131 acute haemolytic anaemia in individuals with glucose-6-phosphate dehydrogenase deficiency (G6PDd).

132 Other abnormal hemoglobins, glucose-6-phosphate dehydrogenase deficiency and pyruvat

133 [95% confidence interval {CI}, 0.52-0.90]), glucose-6-phosphate dehydrogenase deficiency in female c

134 Glucose-6-phosphate dehydrogenase deficiency serves as a

135 lpha-thalassemia, 0.3%; ABO group, 0.3%; and glucose-6-phosphate dehydrogenase deficiency, 0.5%) and

136 tors for neurotoxicity, such as prematurity, glucose-6-phosphate dehydrogenase deficiency, or hypoxia

137 t Asian ovalocytosis and two common forms of glucose-6-phosphate dehydrogenase deficiency.

138 Patients with glucose-6-phosphate dehydrogenase enzyme activity of les

139 ith uncomplicated falciparum malaria, normal glucose-6-phosphate dehydrogenase enzyme levels, and hem

140 A large excess of ALDH3A1 also protected glucose-6-phosphate dehydrogenase from inactivation beca

141 hibition of the pentose phosphate pathway by glucose-6-phosphate dehydrogenase inhibitors and siRNA s

142 e did not observe changes in the activity of glucose-6-phosphate dehydrogenase or in the pentose phos

143 ococcal mutants deficient in PavA, CodY, and glucose-6-phosphate dehydrogenase pointing to the robust

144 METHODS AND Patients with normal glucose-6-phosphate dehydrogenase status with symptomati

145 ecific inhibitor (dehydroepiandrosterone) of glucose-6-phosphate dehydrogenase together established r

146 strain over-expressing zwf gene (coding for glucose-6-phosphate dehydrogenase), WX-zwf, produced the

147 blood cell polymorphisms (ie, hemoglobin S, glucose-6-phosphate dehydrogenase, and alpha-thalassemia

148 three enzymes (catechol-O-methyltransferase, glucose-6-phosphate dehydrogenase, and glyceraldehyde-3-

149 either 6PGD or another oxidative PPP enzyme, glucose-6-phosphate dehydrogenase, exhibit non-immune he

150 mmed RA T cells includes glycolytic enzymes (glucose-6-phosphate dehydrogenase, phosphofructokinase),

151 of the cytosolic isocitrate dehydrogenase or glucose-6-phosphate dehydrogenase, which also produce cy

152 In P. falciparum , the bifunctional enzyme glucose-6-phosphate dehydrogenase-6-phosphogluconolacton

153 oncomitant inhibition of the parasite enzyme glucose-6-phosphate dehydrogenase-6-phosphogluconolacton

154 Conditional expression of the glucose-6-phosphate dehydrogenase-encoding gene zwf, sho

155 placebo-controlled study, 16 malaria-naive, glucose-6-phosphate dehydrogenase-normal participants ag

156 red lactate dehydrogenase and heat-denatured glucose-6-phosphate dehydrogenase.

157 aemia, and a mutation of G6PD, which encodes glucose-6-phosphate dehydrogenase.

158 ence of 6-aminonicotinamide, an inhibitor of glucose-6-phosphate dehydrogenase.

159 ntapeptide derived from the metabolic enzyme glucose-6-phosphate dehydrogenase.

160 sses hexokinase and the rate-limiting enzyme glucose-6-phosphate dehydrogenase.

161 r non-specific glycolytic proteins such as d-glucose-6-phosphate dehydrogenase.

162 In addition, glucose-6-phosphate-dehydrogenase (G6PD) deficiency, whi

163 No correlation with sickle cell trait or glucose-6-phosphate-dehydrogenase deficiency was observe

164 xis to induce expression of hexokinase (HK), glucose-6-phosphate dehyrogenase (G6PD) and pyruvate kin

165 osteric activators (fructose-6-phosphate and glucose-6-phosphate) did not always mimic the changes ob

166 able to isomerize fructose-6-phosphate into glucose-6-phosphate even in the presence of equimolar am

167 ic glucose production by failing to redirect glucose-6-phosphate flux from production of glucose to g

168 pproximately 7-fold higher concentrations of glucose 6-phosphate for the release of HKI.

169 found evidence that carbon is reimported as glucose-6-phosphate, forming a cytosolic bypass around t

170 Diabetes elevated glucose 6-phosphate, fructose 6-phosphate and oxidised (

171 I) and phosphoglucose mutase interconverting glucose 6-phosphate, fructose 6-phosphate, and glucose 1

172 sphate and sedoheptulose 1-phosphate but not glucose 6-phosphate, fructose 6-phosphate, and sedoheptu

173 Glucose 6-phosphate (G-6P), a product of the catalytic a

174 phosphocreatine (PCr) turnover but increased glucose-6-phosphate (G-6-P) turnover, glucose utilizatio

175 , in general, glucose metabolism at least to glucose-6-phosphate (G-6-P).

176 ations were increased 2.6-fold in DMG, while glucose 6-phosphate (G6-P) was unchanged.

177 ccomplished by the small molecule effectors, glucose 6-phosphate (G6P) and fructose 1,6-bisphosphate

178 ndidate mechanisms by which metformin lowers glucose 6-phosphate (G6P) in mouse and rat hepatocytes c

179 Glucose 6-phosphate (G6P) is a metabolic intermediate wi

180 se-6-phosphatase catalyzes the hydrolysis of glucose 6-phosphate (G6P) to glucose and inorganic phosp

181 se monophosphate inhibitors or the activator glucose 6-phosphate (G6P) to MtbPYK tightly regulates th

182 iac glycolysis and explored the potential of glucose 6-phosphate (G6P) to regulate glycolytic flux an

183 ion of beta-glucose 1-phosphate (betaG1P) to glucose 6-phosphate (G6P) using Asp8 of the core domain

184 beta-D-glucose 1-phosphate (betaG1P) into D-glucose 6-phosphate (G6P) via sequential phosphoryl tran

185 ate (betaG1P) derived from maltose to beta-d-glucose 6-phosphate (G6P).

186 x interplay between the allosteric activator glucose-6-phosphate (G6P) and reversible phosphorylation

187 Based on the reaction of glucose-6-phosphate (G6P) and the diaphorase-resazurin a

188 acterium tuberculosis (Mtb) PYK uses AMP and glucose-6-phosphate (G6P) as synergistic allosteric acti

189 Insulin reduced gluconeogenic flux to glucose-6-phosphate (G6P) but only at the near-maximal p

190 G6PT translocates glucose-6-phosphate (G6P) from the cytoplasm into the lu

191 se-beta (G6Pase-beta or G6PC3) that converts glucose-6-phosphate (G6P) into glucose, the primary ener

192 gluconeogenesis and glycogenolysis, in which glucose-6-phosphate (G6P) is hydrolyzed to glucose for r

193 Consistent with a glucose-6-phosphate (G6P) metabolism deficiency, G6pc3(-

194 Tps1 integrates glucose-6-phosphate (G6P) metabolism with nitrogen sourc

195 a like Escherichia coli, the accumulation of glucose-6-phosphate (G6P) or its analogs such as alpha-m

196 d previously that increased carbon flux from glucose-6-phosphate (G6P) through the pentose phosphate

197 se-6-phosphatase catalyzes the hydrolysis of glucose-6-phosphate (G6P) to glucose and inorganic phosp

198 alpha (G6Pase-alpha or G6PC) that hydrolyzes glucose-6-phosphate (G6P) to glucose.

199 Ib (GSD-Ib) is caused by deficiencies in the glucose-6-phosphate (G6P) transporter (G6PT) that have b

200 Ib (GSD-Ib) is caused by a deficiency in the glucose-6-phosphate (G6P) transporter (G6PT) that works

201 meostasis resulting from a deficiency in the glucose-6-phosphate (G6P) transporter (G6PT).

202 colorimetric assay for the determination of glucose-6-phosphate (G6P) was developed.

203 sphates, such as glycerol-3-phosphate (G3P), glucose-6-phosphate (G6P), and fosfomycin.

204 t (Arg582Ala) that could not be activated by glucose-6-phosphate (G6P), but possessed full catalytic

205 primary intracellular metabolite of glucose, glucose-6-phosphate (G6P), on bile acid metabolism.

206 in secretion (GSIS) that acts by hydrolyzing glucose-6-phosphate (G6P), thereby reducing glycolytic f

207 rom mtATP to cytoplasmic glucose to generate glucose-6-phosphate (G6P), which is an established Mondo

208 se enzymes catalyze conversion of glucose to glucose-6-phosphate (G6P), which is the first step in th

209 Studies on Glucose-6-phosphate (G6P)/phosphate translocator isoform

210 ine, fructose, glucose, glucose-1-phosphate, glucose-6-phosphate, galactose, lactose, and sucrose--at

211 e kinase that is allosterically activated by glucose 6-phosphate (Glc-6-P) and adenosine monophosphat

212 e allosteric inhibition of E. coli FBPase by glucose 6-phosphate (Glc-6-P), the first metabolite prod

213 nd with the cofactor GlcN6P or the inhibitor glucose 6-phosphate (Glc6P) at 1.7 A and 2.2 A resolutio

214 me bound to a naturally occurring inhibitor, glucose 6-phosphate (Glc6P), and a nonnatural activating

215 ites, adenosine 5'-monophosphate (AMP) and d-glucose 6-phosphate (Glucose-P), were detected in a subs

216 tdA is a pyridoxal phosphate-dependent 3-oxo-glucose-6-phosphate:glutamate aminotransferase, and NtdB

217 were responsible for generating two NADH per glucose-6-phosphate (i.e., four electrons were generated

218 Analyses of free glucose and glucose 6-phosphate in milk have until now been dependen

219 k that was stripped of intrinsic glucose and glucose 6-phosphate in order to obtain standards and sam

220 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 ate), and glucose 6-phosphate dehydrogenase (glucose 6-phosphate into NADPH), followed by fluorometri

223 combination with conversion of the formed d-glucose-6-phosphate into mixtures of labeled methyl d-gl

224 poptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway t

225 T2 expression by Suc increases the import of glucose-6-phosphate into the plastids that would repress

226 zyme-catalyzed phosphorylation of glucose to glucose-6-phosphate is a reaction central to the metabol

227 we demonstrate that the enzyme's response to glucose-6-phosphate is controlled by Arg583 and Arg587,

228 Glucose-6-phosphate is extensively degraded by the OPP p

229 phosphate enforces a metabolic switch, where glucose-6-phosphate is routed towards storage carbohydra

230 6.TCR.Calpha(-/-)H-2(b/g7) mice induced anti-glucose 6-phosphate isomerase antibody-dependent chronic

231 elping B cells to produce arthritogenic anti-glucose-6-phosphate isomerase (anti-GPI) autoantibodies.

232 atoid arthritis, autoantibodies specific for glucose-6-phosphate isomerase (GPI) can transfer joint-s

233 Glucose-6-phosphate isomerase (GPI) is the target autoan

234 ceptors (BCRs) with different affinities for glucose-6-phosphate isomerase (GPI) were examined in the

235 vealed a point mutation, Gly-189 --> Glu, in glucose-6-phosphate isomerase (GPI), a glycolytic enzyme

236 e displays oral, in vivo efficacy in a mouse glucose-6-phosphate isomerase (GPI)-induced paw swelling

237 autoimmune arthritis by tracking the fate of glucose-6-phosphate isomerase (GPI)-reactive CD4(+) T ce

238 Immunization with human glucose-6-phosphate isomerase (hG6PI) protein or with se

239 thal phenotype of RNAi-mediated depletion of glucose-6-phosphate isomerase (PGI) in the glucose-deple

240 tive pentose phosphate (OPP) pathway and the glucose-6-phosphate isomerase (PGI) reaction.

241 Finally, two proteins (glucose-6-phosphate isomerase [EC 5.3.1.9] and isoflavon

242 se and reduced deposition of pathogenic anti-glucose-6-phosphate isomerase Abs in the joint (with a r

243 r domain serves as a scaffold for recruiting glucose-6-phosphate isomerase and dehydrogenase.

244 inefficient at taking up the key autoantigen glucose-6-phosphate isomerase and that Msr1-deficient mi

245 uld not be reproduced by increasing the anti-glucose-6-phosphate isomerase antibody load, which demon

246 mber of the IL-1 family, can exacerbate anti-glucose-6-phosphate isomerase autoantibody-induced arthr

247 peroxiredoxin-5, secretoglobin family 1D and glucose-6-phosphate isomerase characterized the LF pheno

248 osure, twice-a-day treatment with 17l in the glucose-6-phosphate isomerase chronic in vivo mouse mode

249 hosphate dehydrogenase, pyruvate kinase, and glucose-6-phosphate isomerase showed IgE-binding for 6%-

250 (2) died in galactose medium as well as when glucose-6-phosphate isomerase was knocked down, suggesti

251 to [6,6'-(3)H]Fru-2,6-P(2) using hexokinase, glucose-6-phosphate isomerase, and 6-phosphofructo-2-kin

252 ormation and autoantibody production against glucose-6-phosphate isomerase, leading to joint inflamma

253 e in the titer of serum antibodies targeting glucose-6-phosphate isomerase, the relevant autoantigen,

254 ransgenic mice specific for the self-antigen glucose-6-phosphate isomerase, we show that autoreactive

255 Glucose-6-phosphate isomerase-specific plasma cells did

256 nt mice had elevated serum concentrations of glucose-6-phosphate isomerase.

257 thritis is induced by autoantibodies against glucose-6-phosphate-isomerase (GPI).

258 .5 +/- 0.5 %ID/g), as early as 1 d after the glucose-6-phosphate-isomerase serum injection, a time po

259 We injected mice with serum containing glucose-6-phosphate-isomerase-specific antibodies to ind

260 nalogous to the Entner-Doudoroff pathway for glucose-6-phosphate: It involves an NAD(+)-dependent SQ

261 tes, this regulation is accomplished through glucose-6-phosphate levels and protein phosphorylation.

262 patic glucose production and reduces hepatic glucose-6-phosphate levels to complete a homeostatic loo

263 ding to an approximately twofold increase in glucose-6-phosphate levels.

264 -> UDP-glucose <--> glucose 1-phosphate <--> glucose 6-phosphate <--> fructose 6-phosphate, showed a

265 nd glucose uptake determined through 2-deoxy glucose 6 phosphate luminescence.

266 pathway suggests that in addition to sensing glucose 6-phosphate, MondoA can also sense glucosamine 6

267 catalyze the biosynthesis of kanosamine from glucose-6-phosphate: NtdC is a glucose-6-phosphate 3-deh

268 sitol is generated by de novo synthesis from glucose 6-phosphate or is provided from the environment

269 Some bacteria experience stress when glucose-6-phosphate or analogues like alpha-methyl gluco

270 The glucose-6-phosphate/phosphate antiporter GPT1 is a major

271 transfer to sucrose stimulates expression of GLUCOSE-6-PHOSPHATE/PHOSPHATE TRANSPORTER2 (GPT2) and re

272 ADP-dependent glucokinase (ADPGK) catalyzes glucose-6-phosphate production, utilizing ADP as a phosp

273 However, this also stimulates a glucose-6-phosphate shunt, which consumes ATP, which can

274 combined with fosfomycin in the presence of glucose-6 phosphate, significant synergy is observed.

275 ing isolated intact liver or fat microsomes, glucose-6 phosphate stimulated 11 beta-HSD1 oxo-reductas

276 n storage phenotype by genetic inhibition of glucose-6-phosphate-stimulated glycogen synthase activit

277 Susceptibility testing was performed using a glucose-6-phosphate-supplemented fosfomycin Etest and Ki

278 lator of basal GSIS that acts by hydrolyzing glucose-6-phosphate, thereby reducing glycolytic flux.

279 P-glucuronate) stemmed from UDP-glucose, not glucose 6-phosphate; therefore, UDP-glucuronate arose pr

280 he de novo synthesis is the isomerization of glucose 6-phosphate to 1-D-myo-inositol-3-phosphate, cat

281 t equatorial transamination of 3-oxo-alpha-D-glucose 6-phosphate to form alpha-D-kanosamine 6-phospha

282 by decreased ability of the liver to convert glucose-6-phosphate to glucose leading to glycogen accum

283 synthase (MIPS) catalyzes the conversion of glucose-6-phosphate to myo-inositol-1-phosphate.

284 ffect was blocked by selective inhibitors of glucose-6-phosphate transport.

285 y a deficiency in the ubiquitously expressed glucose 6-phosphate transporter (Glc-6-PT).

286 ense oligonucleotides (ASOs) specific to the glucose 6-phosphate transporter-1 (G6PT1) enabled reduct

287 e disease type-Ib (GSD-Ib), deficient in the glucose-6-phosphate transporter (G6PT), is characterized

288 by a deficiency in a ubiquitously expressed glucose-6-phosphate transporter (G6PT).

289 tid, on the one hand, and up-regulation of a GLUCOSE-6-PHOSPHATE TRANSPORTER (GPT2), on the other han

290 omal-recessive disease caused by mutation of glucose-6-phosphate transporter and characterized by alt

291 this question, we investigated the effect of glucose-6-phosphate transporter mutation on immune cell

292 tients with genetic deficiency in either the glucose-6-phosphate transporter of the endoplasmic retic

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

295 isomerisation of beta-glucose 1-phosphate to glucose 6-phosphate via beta-glucose 1,6-bisphosphate.

296 he postulated competing pathway leading from glucose 6-phosphate via myo-inositol.

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.