ライフサイエンスコーパス: GLUT1

1 n and identified glucose transporter type 1 (GLUT1).

2 SS1) and glucose transporter protein type 1 (GLUT1).

3 synthetic pathway and glucose transporter 1 (GLUT1).

4 vator p300 as well as glucose transporter 1 (Glut1).

5 ansport activity via the glucose transporter GLUT1.

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

7 and expression of the HIF1alpha target gene GLUT1.

8 is activity is predominantly mediated by the Glut1.

9 cose-derived biomass, depending partially on Glut1.

10 resses expression of the glucose transporter Glut1.

11 ORC1 signaling, glycolysis and expression of Glut1.

12 hanced expression of the glucose transporter GLUT1.

13 it isoform selectivity with little effect on GLUT1.

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

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

16 rocytes, causing a decrease of expression of GLUT1.

17 glucose uptake, which is mainly dependent on Glut1.

18 4, with an IC(50) value of low nanomolar for GLUT1.

19 rapamycin, we screened for new inhibitors of GLUT1.

20 ines-were greatly elevated in the absence of GLUT1.

21 estinal sugar transporters, SGLT1 and GLUTs (GLUT1, 2 and 5).

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

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

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

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

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

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

28 rrent deletion of the glucose transporter 1 (Glut1), also known as solute carrier family 2, facilitat

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

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

31 However, most bloodstream cells contain GLUT1 and are not directly affected by insulin.

32 ings pave the way for combined inhibition of GLUT1 and ATR/CHK1 as a therapeutic approach for KRAS-dr

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

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

35 In contrast, platelets isolated from GLUT1 and GLUT3 double-knockout (DKO) mice, which lack t

36 -FDG-PET analyses of tumors demonstrate that Glut1 and Glut3 loss decreases glucose uptake, which is

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

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

39 tors of glucose transporters, targeting both GLUT1 and GLUT3.

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

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

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

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

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

45 These results indicate that co-targeting GLUT1 and GSH synthesis may offer a potential therapeuti

46 Testing a drug combination that co-targeted GLUT1 and GSH synthesis, we found that this combination

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

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

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

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

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

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

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

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

55 Expression of the glucose transporter Glut1 and of glycolytic enzymes as well as mitochondrial

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

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

58 e-mRNAs of critical glycolytic genes such as GLUT1 and PKM2.

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

60 y the study of different substrates, such as GLUT1 and SHBG, demonstrating that the posttranslational

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

62 ophoblast had reduced glucose transporter 1 (GLUT1) and glucocorticoid receptor (GR) expression in re

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

64 reases in HXK1, PFK1, glucose transporter 1 (GLUT1), and GLUT3 mRNA expression.

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

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

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

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

69 at variable levels, including Pdx1, Nkx6.1, GLUT1, and PC1/3.

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

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

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

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

74 tically, combined inhibition of ATR/CHK1 and GLUT1 arrested sensitive cells in S-phase and led to the

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

76 These findings implicate GLUT1 as a Delta9-THC target and provide a potential mec

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

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

79 emonstrate that RgA is a potent inhibitor of GLUT1 as well as GLUT3 and GLUT4, with an IC(50) value o

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

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

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

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

84 , our findings suggest that although lack of GLUT1 blunted glycolysis and the pentose phosphate pathw

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

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

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

88 , also called MCT4), and SLC2A1 (also called GLUT1) by immunoblot analyses.

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

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

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

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

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

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

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

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

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

98 rrier (BBB) dysfunction, but whether and how GLUT1 controls EC metabolism and function is poorly unde

99 Inhibition of GLUT1 decreases EC glucose uptake and glycolysis, leadin

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

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

102 Glut1 deficiency in the progenitors leads to osteopetros

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

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

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

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

107 GLUT1 deletion from quiescent adult ECs leads to severe

108 iratory capacity was blunted in MPhi lacking GLUT1, demonstrating an incomplete metabolic reprogrammi

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

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

111 l model and in primary gonadotropes, we show GLUT1-dependent stimulation of glycolysis, but not mitoc

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

113 However, Ldlr(-/-) mice lacking myeloid GLUT1 developed unstable atherosclerotic lesions.

114 of osteoblast lineage cells, and deletion of Glut1 diminished osteoblast differentiation in vitro.

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

116 y thus constitute an effective treatment for Glut1 DS.

117 ive dysfunction and no optimal treatment for Glut1 DS.

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

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

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

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

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

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

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

125 brain bioenergetics profile in patients with GLUT1-DS.

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

127 the effect was essentially abolished without Glut1, even though transient deletion of Glut1 itself di

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

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

130 dotropin Luteinizing Hormone is supported by GLUT1 expression and activity, and GnRH-induced glycolys

131 nt with the in vivo results, Wnt7b increased Glut1 expression and glucose consumption in the primary

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

133 GnRH stimulation increases gonadotrope GLUT1 expression and translocation to the extracellular

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 By manipulating glucose utilization and GLUT1 expression in a pituitary gonadotrope cell model a

137 Considering that normal GLUT1 expression in oligodendrocytes and myelin is neede

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

139 nt, endothelial glycolysis is repressed, and GLUT1 expression increases in a Notch-dependent fashion.

140 GLUT1 expression increases in vivo during the GnRH-induc

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

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

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

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

145 GLUT1 expression quantification did not significantly di

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

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

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

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

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

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

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

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

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

155 nced by elevated resting glucose and reduced GLUT1 expression.

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

157 tor (HIF)-1 alpha and glucose transporter 1 (Glut1) expression for proinflammatory cytokine productio

158 iciency enhanced glucose transporter type 1 (GLUT1) expression in the liver and also up-regulated GLU

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

160 Deletion of GLUT1 from the developing postnatal retinal endothelium

161 Loss of TCR, CD8, and GLUT1 gave rise to defects in T cell signaling and proli

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

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

164 ng gene KCNN4, and SLC2A1, which encodes the Glut1 glucose transporter.

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

166 1B 19-kDa protein-interacting protein 3) and GLUT1 (glucose transporter 1); (ii) secretion of pre-for

167 GLUT1 (glucose transporter isoform 1/Slc2a1) is highly e

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

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

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

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

172 IVAS also up-regulated GLUT1, GLUT4, and PI3K p85alpha protein, and increased p

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

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

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

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

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

178 ncreased expression of key glycolytic genes (GLUT1, HK2, TPI, and MCT4); activation of AMPK by AICAR

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

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

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

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

183 1291 treatment reduced the protein levels of GLUT1 in both AsPC-1 and PANC-1 cells, leading to a lowe

184 We evaluated the role of GLUT1 in endothelial metabolism and function during post

185 d by higher expression of EOMES, blimp1, and Glut1 in Gal-9(+) versus Gal-9(-) T cells, which is cons

186 predominant SLC2 species expressed alongside GLUT1 in many tissues, but GLUT8 mRNA exists mostly as a

187 Genetic deletion of Glut1 in osteoclast progenitors reduces aerobic glycolys

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

189 Expression of the glucose transporter (GLUT1) in oligodendrocytes was assessed by immunocytoche

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

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

192 dendrocyte expression of glucose transporter GLUT1 induced by NMDAR activity.

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

194 s under conditions of glucose deprivation or GLUT1 inhibition to inhibition of BRPF2/3 BRDs.

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

196 both leader and follower cells with PDH and GLUT1 inhibitors, respectively, inhibits cell growth and

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

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

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

200 Endogenous GLUT1 is phosphorylated on S226 in primary endothelial c

201 GLUT1 is the main glucose transporter in ECs and becomes

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

203 out Glut1, even though transient deletion of Glut1 itself did not affect normal bone accrual.

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

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

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

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

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

209 RK1/2 phosphorylation, higher HIF-1alpha and Glut1 levels, and substantially increased IL-1beta as we

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

211 roarray and confirmed one hit as a bona fide GLUT1 ligand, which we named rapaglutin A (RgA).

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

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

214 Interrogating the GLUT1 mechanism using WZB117 reveals that subsaturating

215 and chemotherapy through targeting ASS1- and GLUT1-mediated arginolysis and glycolysis, respectively,

216 Thus, Glut1-mediated glucose metabolism through both lactate p

217 fied a novel synergistic interaction between GLUT1-mediated glucose transport and the cell-cycle chec

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

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

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

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

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

223 ensable for the maintenance of TCR, CD8, and GLUT1 membrane proteins at the plasma membrane of CTLs,

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

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

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

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

228 ed glycolysis in T cells and decreased their Glut1 mRNA expression.

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

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

231 HCC827 or A549 cells, by decreasing SLC2A1 (GLUT1) mRNA and protein levels and by inhibiting glucose

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

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

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

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

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

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

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

239 Combined inhibition of CHK1/GLUT1 or ATR/GLUT1 robustly induced apoptosis, particula

240 ly one highly expressed glucose transporter, Glut1 or Glut3, in cancer cells does not impair tumor gr

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

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

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

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

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

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

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

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

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

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

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

252 Whether GLUT1 reduction influences disease pathogenesis remains,

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

254 Timely Glut1 repletion may thus constitute an effective treatme

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

256 Our findings demonstrate that GLUT1 reserves and mitochondrial fitness of CD8(+) T cel

257 reduced intracellular glucose transporter 1 (GLUT1) reserves, and have an altered mitochondrial metab

258 In fact, only 12% of GLUT1 resolved into a highly mobile subpopulation.

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

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

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

262 Combined inhibition of CHK1/GLUT1 or ATR/GLUT1 robustly induced apoptosis, particularly in RAS-mu

263 In vivo, simultaneous inhibition of ATR and GLUT1 significantly reduced tumor volume gain in an auto

264 odel of myeloid-specific glucose transporter GLUT1 (Slc2a1) deletion.

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

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

267 urface expression of the glucose transporter GLUT1/Slc2a1.

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

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

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

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

272 romer recruitment to endosomal membranes and GLUT1 surface recycling.

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

274 osamine-coated NISV, for blood-brain barrier GLUT1 targeting, capable of traversing the barrier and d

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

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

277 regulation of the glucose transporter (GLUT) GLUT1 to facilitate increased glucose uptake and glycoly

278 provides rationale for co-targeting PDH and GLUT1 to inhibit collective invasion.

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 Increased levels of GLUT1 transcripts, and upregulation of GAPDH expression

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

285 more slowly than the constitutively secreted GLUT1 transporter and localize CHC22 to the ER-to-Golgi

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

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

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

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

290 rotein levels to be increased 7.8-fold while GLUT1 was decreased 1.7-fold in nerve damaged TA.

291 IUGR-AR skeletal muscle than in controls but GLUT1 was greater in IUGR-AR.

292 2+), a significant increase in cell membrane GLUT1 was measured, thus providing a cellular effect sim

293 n marker mannose receptor CD206, yet lack of GLUT1 was not a critical mediator in the development of

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

295 y antigen (DARC), glycophorin A, band 3, and GLUT1 were compared under analogous conditions on intact

296 cells highly express glucose transporter 1 (GLUT1), which sustains an elevated level of glucose upta

297 gh-dose progesterone inhibited expression of Glut1, which facilitated glucose transport into the cyto

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

299 The glucose transporter 1 (GLUT1) with high expression in cancer cells was approved

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