ライフサイエンスコーパス: GLUT1

1 resses expression of the glucose transporter Glut1.

2 ORC1 signaling, glycolysis and expression of Glut1.

3 hanced expression of the glucose transporter GLUT1.

4 it isoform selectivity with little effect on GLUT1.

5 f the glucose transporters SGLT1, SGLT2, and GLUT1.

6 (HIF-1alpha) and its transcriptional target GLUT1.

7 nd liver, respectively, stain positively for GLUT1.

8 ansport activity via the glucose transporter GLUT1.

9 eased gene expression of glucose transporter GLUT1.

10 pression was 20,000-fold lower compared with GLUT1.

11 and expression of the HIF1alpha target gene GLUT1.

12 is activity is predominantly mediated by the Glut1.

13 uman GLUT2 or the glucose transport of human GLUT1-4 or bacterial GlcPSe.

14 ytic pathway genes, glucose transporter 1-4 (Glut1-4), phosphoglycerate kinase 1 and Glucokinase but

15 much greater in tumor than in muscle tissue (GLUT1 50:1), the opposite was found for GLUT5 mRNA expre

16 nvolved in carbohydrate metabolism including GLUT1, a major glucose transporter.

17 Of note, inhibition of GLUT1 activity and/or expression is shown to impair TGF-

18 Whether dynamic aggregation of GLUT1 also occurs in cell types with more modest express

19 al prostate, with immunohistochemistry (anti-GLUT1) also showing comparable staining.

20 d the expression of the glucose transporters GLUT1 and -4 in the muscle and enhanced the activity of

21 ssed by Oil Red O staining, adiponectin, and Glut1 and 4 expression.

22 s both expression of the glucose transporter Glut1 and aerobic glycolysis for Teff cell proliferation

23 GLUT1 transcription and de novo synthesis of GLUT1 and another part dependent on mTOR complex 2-stimu

24 re shown to target GLUT4 preferentially over GLUT1 and block glucose transport.

25 Surface expression of Glut1 and cellular uptake of the fluorescent glucose ana

26 Cell surface GLUT1 and GLUT3 containing GLUT1 TM9 are 4-fold more cat

27 GLUT1 and GLUT3 display allosteric transport behavior.

28 lated to the non-homogeneous distribution of GLUT1 and GLUT3 in the brain.

29 ake of MAN-LIP was significantly improved by GLUT1 and GLUT3 overexpression cells.

30 ined data indicated that the transcytosis by GLUT1 and GLUT3 was a pathway of MAN-LIP into brain, and

31 r LV-GLUT3/ bEND.3 cell monolayers, of which GLUT1 and GLUT3 were overexpressed.

32 ing transmembrane and cytosolic domains from GLUT1 and GLUT4 and/or point mutations were generated an

33 1) The WZB117 binding envelopes of exofacial GLUT1 and GLUT4 conformers differ significantly.

34 2) GLUT1 and GLUT4 exofacial conformers present multiple, a

35 Despite 68% homology between GLUT1 and GLUT4, our virtual screen identified two poten

36 f glucose by increasing the translocation of GLUT1 and GLUT4.

37 cells, tumors, and muscle and correlated to GLUT1 and GLUT5 expression levels.

38 bstrate selectivity of XylE is compared with GLUT1 and GLUT5, as well as a XylE mutant that transport

39 o proteins important for glucose metabolism, Glut1 and Hexokinase 2 (HXK2).

40 Akt/mTORC1 signaling, reduced expression of Glut1 and hexokinase 2, and decreased glucose metabolism

41 reased expression of the glucose transporter Glut1 and hexokinase 2, and reduced glucose uptake.

42 ith low glucose concentrations led to higher GLUT1 and hexokinase-2 expression as well as higher esti

43 sistent with the messenger RNA expression of GLUT1 and hexokinase-2: culturing with low glucose conce

44 of CF patients had higher levels of PiT1 and Glut1 and increased glucose uptake compared with their b

45 ectly, by binding to the glucose transporter GLUT1 and inducing GLUT1 internalization through clathri

46 cer cells decreased the expression levels of Glut1 and inhibited glycolysis in cancer cells.

47 Changes in Glut1 and Mcl-1 levels, glucose uptake and B cell number

48 feration in GH3 cells via down regulation of Glut1 and MMP2 expression and inhibition of the Akt-GSK-

49 Therefore, SALL4 promotes the expression of Glut1 and open chromatin through a HP1alpha-dependent me

50 ethering these proteins to the N-terminus of GLUT1 and performing saturation BRET analysis, we were a

51 infection, oral steroid treatment decreased Glut1 and PiT2 levels in blood neutrophils.

52 Correlation between GLUT1 and pS6RP levels in tumors was observed but elevat

53 ivated expression of the glucose transporter GLUT1 and repressed expression of the tumor suppressor B

54 GLUT1 and the neuronal glucose transporter GLUT3 do not

55 gar transporter glucose transport protein 1 (GLUT1) and examines the transporter isoform specificity

56 d with expressions of glucose transporter-1 (GLUT1) and hexokinase-2 measured by quantitative real-ti

57 glucose transporter 1 (SLC2A1; also known as GLUT1), and VEGFA has been associated with tumor progres

58 ibits HIF1-induced activation of VEGFA, LOX, Glut1, and c-Met genes in a panel of cell lines represen

59 ighly expressed proteins, including basigin, Glut1, and CD98hc.

60 The prognostic significance of CD8A, GLUT1, and COX5B gene expression was analyzed within The

61 ion of the hypoxia-related genes EPO, VEGFA, GLUT1, and END1 in tumors.

62 CAIX, GLUT1, and Ki67 were upregulated in the tumor edge, cons

63 Biomarkers such as pS6RP, GLUT1, and tumor FDG uptake are being evaluated in patie

64 By transplanting bone marrow from WT, Glut1(+/-), ApoE(-/-), and ApoE(-/-)Glut1(+/-) mice into

65 ed and the nonintestinal glucose transporter GLUT1 appeared at the basolateral membrane of enterocyte

66 order of potency: insulin-regulated GLUT4 >> GLUT1 approximately neuronal GLUT3.

67 HIF-1alpha and GLUT1 are critical for OGT-mediated regulation of metabo

68 over, the levels of the glucose transporter, GLUT1, are also reduced compared to wild-type T cells.

69 iral overexpression studies, we have defined GLUT1 as a critical downstream target of HIF-1alpha medi

70 ecific antibodies, we identify serine 226 in GLUT1 as a PKC phosphorylation site.

71 tenance and myelomonocytic fate and suggests Glut1 as potential drug target for atherosclerosis.

72 , we identify SLC2A1 (glucose transporter 1, GLUT1) as a downstream target of DERL3.

73 s characterized by more salient increases in Glut1, ASCT2, PiT1, and PiT2 expression.

74 The glucose transporter GLUT1 at the blood-brain barrier (BBB) mediates glucose

75 Glut1, indicating the importance of HP1alpha-Glut1 axis in SALL4-mediated DDR.

76 f MAN-LIP was much stronger when crossing LV-GLUT1/bEND.3 cell monolayers or LV-GLUT3/ bEND.3 cell mo

77 nsporters, a residue that is a tryptophan in GLUT1 but an alanine in GLUT5.

78 Rubusoside also inhibited human GLUT1, but astragalin-6-glucoside did not.

79 ellular WZB117 does not affect CB binding to GLUT1, but intracellular WZB117 inhibits CB binding.

80 In vivo, lentiviral inhibition of Glut1 by shRNA prevented myeloproliferation and adipose

81 There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatm

82 e lower expression of the nutrient receptors GLUT1, CD71 and CD98, which would increase the need for

83 s attributable to its ability to bind to the GLUT1 channel at a site distinct from that of glucose.

84 ignificantly increased surface expression of Glut1 compared with those from HIV(-) controls.

85 eic breast cancer mouse model overexpressing GLUT1, compound 2 showed antitumor efficacy and selectiv

86 ing the expression of glucose transporter 1 (Glut1), compromising glucose flux, and increasing oxidat

87 Gln-282 contributed to sugar binding in all GLUT1 conformations via hydrogen bonding.

88 sugar transport by confirming at least four GLUT1 conformations, the so-called outward, outward-occl

89 utward-occluded, inward-occluded, and inward GLUT1 conformations.

90 4) The inward GLUT1 conformer presents overlapping endofacial WZB117,

91 We identified that Glut1 connects the enhanced glucose uptake in atheromato

92 old more catalytically active than GLUT3 and GLUT1 containing GLUT3 TM9.

93 Glut3, but not Glut1, correlates with poor survival in brain tumors and

94 transport and a diagnostic criterion for the Glut1 deficiency genetic syndrome.

95 Diagnosis of GLUT1 deficiency has important treatment (ketogenic diet

96 We also show that GLUT1 deficiency in endothelium, but not in astrocytes,

97 Here we show that GLUT1 deficiency in mice overexpressing amyloid beta-pep

98 terolemic ApoE-deficient mice, we found that Glut1 deficiency reversed ApoE(-/-) hematopoietic stem a

99 n and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS).

100 ults of all patients with genetically proven GLUT1 deficiency syndrome described in literature were r

101 y occurring, pathogenic mutations that cause GLUT1 deficiency syndrome disrupt this PKC phosphomotif,

102 ke the existence of a reliable biomarker for GLUT1 deficiency syndrome even more important, in order

103 GLUT1 deficiency syndrome is a treatable neurometabolic

104 A typical CSF profile for GLUT1 deficiency syndrome, which is defined as a CSF glu

105 SF analysis is a reliable screening tool for GLUT1 deficiency syndrome.

106 quate biomarkers in the diagnostic workup of GLUT1 deficiency syndrome.

107 y, not to miss SLC2A1-negative patients with GLUT1 deficiency syndrome.

108 patients who received a diagnosis other than GLUT1 deficiency syndrome.

109 Glucose transporter type 1 (GLUT1) deficiency syndrome (GLUT1-DS) leads to a wide ra

110 that both down-regulated IL-2 signaling and Glut1-dependent glycolytic metabolism contribute to the

111 ese data show that activated B cells require Glut1-dependent metabolic reprogramming to support proli

112 his feedforward regulation between RUNX2 and Glut1 determines the onset of osteoblast differentiation

113 Stokes radius particles, which correspond to GLUT1 dimers and tetramers, respectively.

114 Using homology-scanning mutagenesis in which GLUT1 domains are substituted with equivalent GLUT3 doma

115 ut1 signal transduction or by siRNA-mediated Glut1 down-regulation.

116 pmental disorder, Glut1 deficiency syndrome (Glut1 DS).

117 ive dysfunction and no optimal treatment for Glut1 DS.

118 y thus constitute an effective treatment for Glut1 DS.

119 n only on red blood cells from patients with GLUT1-DS (23 patients; 78%), including patients with inc

120 tment and withdrawal) in eight patients with GLUT1-DS (7-47 years old) with non-epileptic paroxysmal

121 Patients with GLUT1-DS experienced a mean of 30.8 (+/- 27.7) paroxysma

122 test opens perspectives for the screening of GLUT1-DS in children and adults with cognitive impairmen

123 ple and rapid blood test in 30 patients with GLUT1-DS with predominant movement disorders, 18 patient

124 nsporter type 1 (GLUT1) deficiency syndrome (GLUT1-DS) leads to a wide range of neurological symptoms

125 cose transporter type 1 deficiency syndrome (GLUT1-DS) who objected to or did not tolerate ketogenic

126 brain bioenergetics profile in patients with GLUT1-DS.

127 function of the cerebral glucose transporter GLUT1 (encoded by SLC2A1) is known to result in epilepsy

128 ecognized regulator of TCR, CD28, LFA-1, and GLUT1 endosome-to-membrane recycling.

129 GLUT1 exhibits trans-acceleration, in which the presence

130 3) The GLUT1 exofacial conformer lacks a CB binding site.

131 most cell types to some extent, the level of GLUT1 expression across different cell types can vary dr

132 oward aerobic metabolism, with a decrease in GLUT1 expression and an increase in lactate upload via t

133 proportionally increased glucose transporter Glut1 expression and mitochondrial mass upon either LPS

134 glucose transport associated with diminished GLUT1 expression at the BBB.

135 sed glucose metabolism in monocytes and that Glut1 expression by proinflammatory monocytes is a poten

136 d multipotential progenitor cells and higher Glut1 expression in these cells.

137 In addition, enhanced GLUT1 expression is observed in fibrotic areas of lungs

138 Upon prolonged HFD feeding, GLUT1 expression is restored, which is paralleled by inc

139 ls suppressed open chromatin, glycolysis and Glut1 expression levels.

140 We detected significantly reduced GLUT1 expression only on red blood cells from patients w

141 GLUT1 expression quantification did not significantly di

142 In turn, inducible reduction of GLUT1 expression specifically in BECs reduces brain gluc

143 16(+)) monocyte subpopulations showed higher Glut1 expression than did classical (CD14(++)CD16(-)) mo

144 Notably, Glut1 expression was sufficient to increase the number o

145 Thus, reduced BBB GLUT1 expression worsens Alzheimer's disease cerebrovasc

146 IL-7 treatment improved mTOR activation, GLUT1 expression, and glucose entry in septic patients'

147 Moreover, RUNX2 favors Glut1 expression, and this feedforward regulation betwee

148 of VEGF in VEGF(Deltamyel) mice impairs BBB-GLUT1 expression, brain glucose uptake, and memory forma

149 h-density lipoprotein (HDL) levels decreased Glut1 expression, dampened myeloproliferation, and preve

150 o induce glycolysis, OXPHOS, ATP production, GLUT1 expression, glucose entry, and proliferation to si

151 Skp2 deficiency impairs Akt activation, Glut1 expression, glucose uptake and glycolysis, and bre

152 sulfenylation of SIRT6, glucose transporter Glut1 expression, glucose uptake, and glycolysis.

153 We identify the IL-7-induced increase in Glut1 expression, resulting in augmented glucose uptake,

154 cin complex 2, which cooperate in regulating GLUT1 expression.

155 othesis, we evaluated glucose transporter 1 (Glut1) expression and glucose uptake by monocyte subpopu

156 ood-brain barrier glucose transport protein (GLUT1) forms homodimers and homotetramers in detergent m

157 Transport of GLUT1 from endosomes to the cell surface requires VARP,

158 ion of TXNIP results in an acute increase in GLUT1 function and an increase in GLUT1 mRNA (hence the

159 reveal a markedly elevated expression of the GLUT1 glucose transporter in lung SqCC, which augments g

160 f vitamin C, dehydroascorbate (DHA), via the GLUT1 glucose transporter.

161 Recent structural studies suggest that GLUT1 (glucose transporter 1)-mediated sugar transport i

162 1B 19-kDa protein-interacting protein 3) and GLUT1 (glucose transporter 1); (ii) secretion of pre-for

163 ino acids, we compared surface expression of Glut1 (glucose) and ASCT2 (neutral amino acids) transpor

164 RNAs encoding the sugar transporters SGLT1, GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5.

165 dition increased brain glucose transporters, Glut1 & Glut3, greater brain derived neurotrophic factor

166 In contrast to the glucose transporter GLUT1, GLUT3 was regulated by environmental oxygen and l

167 s used to evaluate the relevant transporters GLUT1, GLUT3, and GLUT4 and vitamin C transporters SVCT1

168 ized (13)C-DHA via the glucose transporters (GLUT1, GLUT3, and GLUT4) in TRAMP tumor.

169 Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold t

170 take or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-indu

171 TM9) is necessary for optimal association of GLUT1-GLUT3 chimeras with parental GLUT1 in HEK cells.

172 ox1, Cs, Cycs, Ucp3) and glucose metabolism (Glut1, Glut4, Hk2) was increased.

173 c gene signature (high CD8A, high COX5B, low GLUT1) had improved short- and long-term survival.

174 While GLUT1 has several inhibitors, none have been described f

175 es-which express particularly high levels of GLUT1-have suggested that GLUT1 is able to form tetramer

176 in glucose and choline metabolism including GLUT1, HK2, LDHA and CHKA.

177 in cell types with more modest expression of GLUT1, however, is unclear.

178 bition was associated with the inhibition of GLUT1 (IC(50), 2 muM).

179 Glucose transporter 1 (GLUT1) immunohistochemistry was performed to assess whet

180 Recently, the crystal structure of GLUT1 in an inward open conformation was reported.

181 Mechanistically, the regulation of Glut1 in ApoE(-/-) hematopoietic stem and multipotential

182 iation of GLUT1-GLUT3 chimeras with parental GLUT1 in HEK cells.

183 high levels of the glucose uptake receptor, Glut1 (in the absence of any cytokine), and had higher r

184 ectly phosphorylates the glucose transporter Glut1, in order to promote glucose uptake in response to

185 can be rescued by the restored expression of Glut1, indicating the importance of HP1alpha-Glut1 axis

186 ke and enhanced cell surface localization of GLUT1 induced by the phorbol ester 12-O-tetradecanoyl-ph

187 ke in the absence and in the presence of the GLUT1 inhibitor cytochalasin B, and by comparing their a

188 ecific tumor contexts, the identification of GLUT1 inhibitors via synthetic lethality screens, novel

189 o the glucose transporter GLUT1 and inducing GLUT1 internalization through clathrin-coated pits, as w

190 GLUT4 is sufficient to completely transform GLUT1 into GLUT4 with respect to indinavir inhibition of

191 rly high levels of GLUT1-have suggested that GLUT1 is able to form tetrameric complexes with enhanced

192 ral and transport studies by suggesting that GLUT1 is an oligomer of allosteric, alternating access t

193 cificity of resulting glycoconjugates, where GLUT1 is glucose transporter 1.

194 In the TRAMP model, GLUT1 is not significantly upregulated and is unlikely t

195 Endogenous GLUT1 is phosphorylated on S226 in primary endothelial c

196 n of the facilitative glucose transporter 1 (GLUT1) is induced by TGF-beta in fibroblast lines and pr

197 eir anticancer activity in DU145 cells and a GLUT1 knockdown cell line.

198 h the upregulation of glucose transporter-1 (Glut1), lactate secretion and induced cellular invasion

199 increased expression of glucose transporter GLUT1, lactate production, and extrusion of lactate by d

200 NMDA receptors mobilizes glucose transporter GLUT1, leading to its incorporation into the myelin comp

201 Furthermore, B cell-specific deletion of Glut1 led to reduced B cell numbers and impaired Ab prod

202 Through regulating GLUT1 level, GLD4 affects glucose uptake into cells and

203 se import and surface glucose transporter 1 (GLUT1) levels, leading to elevated glycolysis, oxidative

204 teric), and co-existent, exo- and endofacial GLUT1 ligand-binding sites.

205 tergent solubilized, purified GLUT1 resolves GLUT1/lipid/detergent micelles as 6- and 10-nm Stokes ra

206 logy and cognitive function, suggesting that GLUT1 may represent a therapeutic target for Alzheimer's

207 Interrogating the GLUT1 mechanism using WZB117 reveals that subsaturating

208 resses paraoxonase 2 (PON2), which regulates GLUT1-mediated glucose transport via stomatin.

209 Whereas, Glut1-mediated glucose uptake also requires mTORC2 phosp

210 Here, we directly investigated the role of Glut1-mediated glucose uptake in apolipoprotein E-defici

211 ct physiologic programs related to Glut4 and Glut1-mediated glucose uptake.

212 Clinically, elevated GLUT1-mediated glycolysis in lung SqCC strongly correlat

213 Thus, our studies reveal the Glut1-mediated metabolic pathway as a critical regulator

214 well as indirectly, by reducing the level of GLUT1 messenger RNA (mRNA).

215 reaction showed no significant difference in GLUT1 messenger RNA between TRAMP tumor and normal prost

216 elated with increased and glucose-dependent (GLUT1) metabolism with decreased intratumoral CD8/CD4 ra

217 from WT, Glut1(+/-), ApoE(-/-), and ApoE(-/-)Glut1(+/-) mice into hypercholesterolemic ApoE-deficient

218 ned in autophagy-deficient cells, leading to GLUT1 mis-sorting into endolysosomal compartments.

219 An increase in GLUT1 mRNA (12 h) and protein expression (at 3, 6, and 1

220 ncrease in GLUT1 function and an increase in GLUT1 mRNA (hence the total protein levels) for long-ter

221 vascular endothelial growth factor, HK1, and GLUT1 mRNA in response to hypoxia.

222 GLD4-mediated translational control of GLUT1 mRNA is dependent of an RNA binding protein, CPEB1

223 insights into the physiological relevance of GLUT1 multimerization as well as a new variant of BRET a

224 igh-dose glucosamine significantly decreased Glut1 N-glycosylation in Th1-polarized cells.

225 oaches, we demonstrate that up-regulation of GLUT1 occurs via the canonical Smad2/3 pathway and requi

226 nd proteome profiling analysis revealed that GLUT1-OE MPhis demonstrated a hyperinflammatory state ch

227 sed the GLUT1 transporter in RAW264.7 MPhis (GLUT1-OE MPhis).

228 dative stress were significantly enhanced in GLUT1-OE MPhis; antioxidant treatment blunted the expres

229 nt micelles and in cell membranes, where the GLUT1 oligomeric state determines GLUT1 transport behavi

230 We demonstrate that the phosphorylation of GLUT1 on S226 regulates glucose transport and propose th

231 Lesional vessels did not express GLUT1 or the lymphatic marker D2-40, whereas WT1 was exp

232 s, and radiotracer studies demonstrated that GLUT1 overexpression resulted in elevated glucose uptake

233 easing Akt/mTORC1 signaling or expression of Glut1 partially restored T cell function.

234 sulted in reduced expression levels of Vegf, Glut1, Pgk1, and Col10 compared to control shRNA.

235 distinct functionally defined SV pools via V-Glut1-pHluorin fluorescence in cultured hippocampal neur

236 regulated expression of the glycolytic genes GLUT1, PKM2 and LDHA, and of CDC25A; thus, Cdc25A upregu

237 tromer recruitment to endosome membranes and GLUT1 plasma membrane translocation.

238 Depletion of GLD4 not only reduced GLUT1 poly(A) tail length, but also GLUT1 protein.

239 We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting i

240 reduced GLUT1 poly(A) tail length, but also GLUT1 protein.

241 anslated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neu

242 urther enabled us to estimate the density of GLUT1 proteins required for spontaneous oligomerization.

243 tween FDG uptake and the corresponding Ki67, GLUT1, pS6RP expression in tumor biopsies from patients

244 Whether GLUT1 reduction influences disease pathogenesis remains,

245 nt following symptom onset can be effective; Glut1 repletion in early-symptomatic mutants that have e

246 Timely Glut1 repletion may thus constitute an effective treatme

247 sgenic expression of the glucose transporter Glut1 rescued cytokine production of T cells from fasted

248 stress, as overexpression of stable HIF-1 or GLUT1 rescues metabolic defects.

249 olubilized from HEK cells show that HEK cell GLUT1 resolves as 6- and 10-nm Stokes radius particles,

250 atography of detergent solubilized, purified GLUT1 resolves GLUT1/lipid/detergent micelles as 6- and

251 The glucose influx through GLUT1 restores ATP-to-ADP ratios in the short run and ul

252 BSG1 binds to the glucose transporter GLUT1, resulting in increased glucose entry into cones.

253 dies to define the temporal requirements for Glut1 reveal that pre-symptomatic, AAV9-mediated repleti

254 , based on the crystal structure of hSLC2A1 (GLUT1), reveal that Ile-335 (or the homologous Ile-296 i

255 T cells is abrogated either by impairment of Glut1 signal transduction or by siRNA-mediated Glut1 dow

256 Inhibition of RhoA/ROCK/GLUT1 signalling largely abolishes mutp53 GOF in stimula

257 The facilitated glucose transporter GLUT1 (SLC2A1) is an important mediator of glucose homeo

258 We report that GLUT1 (SLC2A1) is the primary rate-limiting glucose tran

259 urface expression of the glucose transporter GLUT1/Slc2a1.

260 that C2-substituted Glc-Pt 2 has the highest GLUT1-specific internalization, which also reflects the

261 uptake and cytotoxicity profile but also the GLUT1 specificity of resulting glycoconjugates, where GL

262 The GLUT1 specificity of the Glc-Pts was evaluated by determ

263 ess whether (18)F-FDG uptake correlates with GLUT1 staining.

264 romer recruitment to endosomal membranes and GLUT1 surface recycling.

265 se human erythrocytes express high levels of Glut1, take up DHA, and reduce it to VC, we tested how e

266 for the selectivity of PIs toward GLUT4 over GLUT1 that can be used in ongoing novel drug design.

267 Unlike GLUT1 that is highly expressed in cancer and more ubiqui

268 ny important cell surface membrane proteins: GLUT1 (the red cell glucose transporter) and then GLUT2

269 ught after mammalian mechanosensory protein; GLUT1, the glucose transporter; SLC4A1, the anion transp

270 PIEZO1, a mammalian mechanosensory protein; GLUT1, the glucose transporter; SLC4A1, the anion transp

271 thermore, we found that increasing dosage of Glut1-the Drosophila melanogaster homologue of this gluc

272 Cell surface GLUT1 and GLUT3 containing GLUT1 TM9 are 4-fold more catalytically active than GLUT

273 Substitution of GLUT3 TM9 with GLUT1 TM9 causes chimeric GLUT3 to resolve as 6- and 10-

274 Substitution of GLUT1 TM9 with GLUT3 TM9 causes chimeric GLUT1 to resolv

275 GLUT1 TMs 2, 5, 8, and 11 also contribute to a less abun

276 of GLUT1 TM9 with GLUT3 TM9 causes chimeric GLUT1 to resolve as a mixture of 6- and 4-nm particles.

277 Substitution of Thr-30 and His-160 in GLUT1 to the corresponding positions in GLUT4 is suffici

278 timulated translocation of newly synthesized GLUT1 to the plasma membrane, leading to increased gluco

279 reasing translocation of glucose transporter GLUT1 to the plasma membrane.

280 cerebral glucose transporter, in addition to GLUT1, to be involved in neurodevelopmental disability.

281 e autophagy and endosomal pathways dictating GLUT1 trafficking and extracellular nutrient uptake.

282 abolic stress facilitates retromer-dependent GLUT1 trafficking.

283 part dependent on cAMP-mediated increases in GLUT1 transcription and de novo synthesis of GLUT1 and a

284 Increased levels of GLUT1 transcripts, and upregulation of GAPDH expression

285 mulates the Warburg effect through promoting GLUT1 translocation to the plasma membrane, which is med

286 Additional GI accelerated membranous GLUT1 translocation, elevating glucose uptake, and incre

287 We propose that GLUT1 transmembrane domain 6 restrains import when intra

288 t GLUT3 domains and vice versa, we show that GLUT1 transmembrane helix 9 (TM9) is necessary for optim

289 where the GLUT1 oligomeric state determines GLUT1 transport behavior.

290 glucose uptake, we stably overexpressed the GLUT1 transporter in RAW264.7 MPhis (GLUT1-OE MPhis).

291 Glucose transporters GLUT1 (transports glucose) and GLUT5 (transports fructos

292 epletion impairs glucose deprivation-induced GLUT1 up-regulation.

293 pathy associated with glucose transporter-1 (Glut1) up-regulation and a glycolytic shift in lung meta

294 ery was lost in an oligomerization-deficient GLUT1 variant in which we substituted membrane helix 9 w

295 GLUT1 was also evaluated by immunohistochemistry.

296 In contrast, expression of Glut1 was correlated with FDG uptake only in tumors driv

297 Thus, Glut1 was necessary to sustain proliferation and potenti

298 he mRNA expression of glucose transporter 1 (GLUT1) was upregulated but glucose transporter 4 (GLUT4)

299 lasts, is transported in these cells through Glut1, whose expression precedes that of Runx2.

300 f the erythrocyte/brain glucose transporter, GLUT1, without a clear understanding of the site(s) of p