ライフサイエンスコーパス: glucose transporter

1 This effect is mediated by the Glut4 glucose transporter.

2 ohydrate metabolism including GLUT1, a major glucose transporter.

3 In addition, this analysis uncovered a novel glucose transporter.

4 min C, dehydroascorbate (DHA), via the GLUT1 glucose transporter.

5 e KCNN4, and SLC2A1, which encodes the Glut1 glucose transporter.

6 the daughter cell of the mRNA for a specific glucose transporter.

7 conditions and expressing different types of glucose transporters.

8 okinases rather than increased expression of glucose transporters.

9 in the repression of HXT genes, which encode glucose transporters.

10 susceptibility to inhibition of polycomb and glucose transporters.

11 ane-associated transporters are described as glucose transporters.

12 lls utilize members of a conserved family of glucose transporters.

13 entify the ubiquitination sites within these glucose transporters.

14 ts targeted arsenic-dependent degradation of glucose transporters.

15 sults were supported by significantly higher glucose transporter 1 (Glut-1) expression of CD4+ cells

16 or-activated receptor gamma (PPAR-gamma) and glucose transporter 1 (GLUT-1) levels in human brain mic

17 HIF-1alpha, and its downstream proteins, glucose transporter 1 (GLUT-1), erythropoietin (EPO), an

18 smooth muscle actin (SMA), D2-40, CD34, and glucose transporter 1 (GLUT-1).

19 , at E19.5 labyrinth trophoblast had reduced glucose transporter 1 (GLUT1) and glucocorticoid recepto

20 To test this hypothesis, we evaluated glucose transporter 1 (Glut1) expression and glucose upt

21 y hypoxia-inducible factor (HIF)-1 alpha and glucose transporter 1 (Glut1) expression for proinflamma

22 Glucose transporter 1 (GLUT1) immunohistochemistry was p

23 we show that expression of the facilitative glucose transporter 1 (GLUT1) is induced by TGF-beta in

24 tant increases in glucose import and surface glucose transporter 1 (GLUT1) levels, leading to elevate

25 +) T cells in CLL have reduced intracellular glucose transporter 1 (GLUT1) reserves, and have an alte

26 nd lipolysis (17.7%); the mRNA expression of glucose transporter 1 (GLUT1) was upregulated but glucos

27 The glucose transporter 1 (GLUT1) with high expression in ca

28 , with or without concurrent deletion of the glucose transporter 1 (Glut1), also known as solute carr

29 RNA expression, and decreases in HXK1, PFK1, glucose transporter 1 (GLUT1), and GLUT3 mRNA expression

30 depleted LICs by reducing the expression of glucose transporter 1 (Glut1), compromising glucose flux

31 In contrast, follower cells highly express glucose transporter 1 (GLUT1), which sustains an elevate

32 novo serine-glycine biosynthetic pathway and glucose transporter 1 (GLUT1).

33 transcriptional co-activator p300 as well as glucose transporter 1 (Glut1).

34 energy, leading to increased levels of human glucose transporter 1 (hGLUT1).

35 tration (20%) of the nonmetabolizable sodium-glucose transporter 1 (SGLT1) substrate, methyl-alpha-D-

36 hypoxia-inducible factor 1alpha (HIF1alpha), glucose transporter 1 (SLC2A1; also known as GLUT1), and

37 Furthermore, the expression of both glucose transporter 1 and hexokinase 2, the first enzyme

38 sion of hypoxia-inducible factor 1-alpha and glucose transporter 1 and increased glucose uptake.

39 l death and that pharmacologic inhibition of glucose transporter 1 and PRC1 synergistically promoted

40 Profibrotic up-regulation of glucose transporter 1 by TGF-beta involves activation of

41 n CD46-costimulated T cells and identify the glucose transporter 1 encoding transcript SLC2A1 as a ta

42 kers of proliferation (K(i)-67) and hypoxia (glucose transporter 1) defined metabolic signaling in th

43 ecent structural studies suggest that GLUT1 (glucose transporter 1)-mediated sugar transport is media

44 Da protein-interacting protein 3) and GLUT1 (glucose transporter 1); (ii) secretion of pre-formed IL-

45 ith upregulation of the glucose transporter, glucose transporter 1, and glycolytic genes, hk1 and pdk

46 he expression of the HIF-1alpha-target gene, glucose transporter 1, and report that HIF-1alpha promot

47 ression of hypoxia-inducible factor 1 alpha, glucose transporter 1, and vascular endothelial growth f

48 Although glucose transporter 1, claudin-3, and plasmalemma vesicu

49 ntial proteome analysis, we identify SLC2A1 (glucose transporter 1, GLUT1) as a downstream target of

50 2 and the cerebrovascular-selective proteins glucose transporter 1, permeability-glycoprotein, and la

51 ed upregulation of glycolytic pathway genes, glucose transporter 1-4 (Glut1-4), phosphoglycerate kina

52 ivity were markedly increased as a result of glucose transporter 1-mediated glucose influx that drive

53 RC2 to drive glycolysis and lipogenesis, and glucose transporter 1-mediated glucose metabolism promot

54 ze, non-signet ring cell carcinoma type, and glucose transporter 1-positive expression on immunohisto

55 of resulting glycoconjugates, where GLUT1 is glucose transporter 1.

56 Mechanistically, glucose uptake via GLUT (glucose transporter)-1 and enhanced glycolysis in neutro

57 parameters were compared with expressions of glucose transporter-1 (GLUT1) and hexokinase-2 measured

58 e and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain fun

59 d glucose uptake through the upregulation of glucose transporter-1 (Glut1), lactate secretion and ind

60 on of glucose transporters (sodium-dependent glucose transporter-1 and glucose transporter-2) and swe

61 Glucose transporter-1 and Ki-67 were negative in the end

62 tilization accompanies the downregulation of glucose transporter-1 and poly (ADP-ribose) polymerase c

63 Proof-of-concept microCT and glucose transporter-1 staining served as morphologic val

64 expression of the HIF-1alpha targets VEGF-A, glucose transporter-1, and lactate dehydrogenase A.

65 nd expression of intestinal sodium-dependent glucose transporter-1, glucose transporter-2, and sweet

66 of high SUVmax, with an increased number of glucose transporter-1-positive cells.

67 ll line system, which found up-regulation of glucose transporter 2 (GLUT2) and glycogen synthase 2 (G

68 ed glucose reabsorption via the facilitative glucose transporter 2 (GLUT2) during diabetes may lead t

69 Here, we studied mice with inactivation of glucose transporter 2 (Glut2) in the nervous system (NG2

70 nd uncovered several target genes, including glucose transporter 2 (Glut2), MAF BZIP transcription fa

71 levels and body weight by inhibiting sodium glucose transporter 2 (SGLT2) in proximal tubular cells.

72 Incubation of mouse islets with the sodium glucose transporter 2 inhibitor dapagliflozin induced pr

73 ted by inflammation, via IL1B, and by sodium glucose transporter 2.

74 synthetase (3), and glucose transport genes (glucose transporter-2 and insulin receptor) in the jejun

75 diabetes, despite dual inhibition of sodium-glucose transporter-2 and the renin-angiotensin system,

76 In summary, sodium-glucose transporter-2 inhibition with empagliflozin redu

77 may derive even greater benefit from sodium glucose transporter-2 inhibitor therapy.

78 Sodium glucose transporter-2 inhibitors reduce the risk of majo

79 firm the large clinical benefits with sodium glucose transporter-2 inhibitors we observed in patients

80 (sodium-dependent glucose transporter-1 and glucose transporter-2) and sweet taste receptor transcri

81 inal sodium-dependent glucose transporter-1, glucose transporter-2, and sweet taste receptors in huma

82 basis, the glucose transport carried out by glucose transporter 3 (GLUT3) was downregulated in TKI-s

83 well as subsequent increase in the neuronal glucose transporter 3 (Glut3), underlies this glycolysis

84 r 3 (SLC2A3) which encodes the high-affinity glucose transporter 3 (GLUT3).

85 of obese rats: reductions in adiponectin and glucose transporter 4 (GLUT 4) and increases in dipeptid

86 termined by key adipocyte markers, including glucose transporter 4 (GLUT4) and adiponectin expression

87 responsive amino peptidase (IRAP) along with glucose transporter 4 (Glut4) and sortilin, represents a

88 at cells by inducing a net redistribution of glucose transporter 4 (GLUT4) from intracellular storage

89 ly increased plasma membrane localization of glucose transporter 4 (GLUT4) in skeletal muscle and adi

90 Glucose transporter 4 (GLUT4) is sequestered inside musc

91 ked glucose uptake by 1 h into G(1) Of note, glucose transporter 4 (glut4) localized on the RMC surfa

92 -genetics screen based on translocation of a glucose transporter 4 (Glut4) reporter expressed in muri

93 Insulin-dependent translocation of glucose transporter 4 (Glut4) to the plasma membrane pla

94 ulin receptor (IR) and the redistribution of glucose transporter 4 (GLUT4) to the plasma membrane.

95 into skeletal muscle through recruitment of glucose transporter 4 (GLUT4) to the plasma membrane.

96 ing augments glucose transport by regulating glucose transporter 4 (GLUT4) trafficking from specializ

97 Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR

98 se transporter 1 (GLUT1) was upregulated but glucose transporter 4 (GLUT4) was unaffected, and adipos

99 activate the insulin-responsive facilitative glucose transporter 4 (GLUT4).

100 g demonstrated a 60% elevation of myocardial glucose transporter 4 expression in the left ventricle a

101 ng protein that regulates the trafficking of glucose transporter 4 in response to insulin and muscle

102 gested to be required for insulin-stimulated glucose transporter 4 translocation in mouse skeletal mu

103 by stimulating the membrane translocation of glucose transporter 4.

104 differentiated C2C12 myotubes by stimulating glucose transporter-4 (GLUT-4) membraned translocation.

105 im of this study was to evaluate the role of glucose transporter-4 (GLUT4) in the anti-diabetic effec

106 The role of insulin-regulated glucose transporter-4 (GluT4) in the brain is unclear.

107 The insulin-regulated glucose transporter-4 (GluT4) is critical for insulin- a

108 ride lipase enzymes, leptin, adiponectin and glucose transporter-4 in 3T3-L1 cells which may have con

109 stinal fructose uptake is mainly mediated by glucose transporter 5 (GLUT5/SLC2A5).

110 (3) H]methyl-d-glucose and placental SLC2A8 (glucose transporter 8) gene expression were also greater

111 Human glucose transporter 9 (hSLC2A9) is an essential protein

112 an and rat nephrons (with the exception of a glucose transporter along the proximal tubule and the H+

113 n resistance, lower brain glucose uptake and glucose transporters, alterations in glycolytic and acet

114 he Drosophila melanogaster homologue of this glucose transporter-ameliorated HD-relevant phenotypes i

115 also displayed significant downregulation of glucose transporter and glycolytic gene expression point

116 is was associated with reduced expression of glucose transporters and glycolytic enzymes in cultured

117 explained by transcriptional upregulation of glucose transporters and glycolytic enzymes(3-5), it is

118 ing its ability to repress the expression of glucose transporters and glycolytic enzymes, inhibiting

119 endocytosis of both the Hxt1, Hxt3, and Hxt6 glucose transporters and the Jen1 lactate transporter.

120 pplication of these studies to understanding glucose transporters and their interaction with substrat

121 y an increased glucose uptake, expression of glucose transporter, and glycolytic enzymes.

122 med, including Western blot, cell migration, glucose transporter, and hexokinase assays (paired t tes

123 ranslocation of vesicles containing GLUT4, a glucose transporter, and insulin-regulated aminopeptidas

124 ect on the sodium independent GLUT family of glucose transporters, and the most potent ones were not

125 Glucose transporters are central players in glucose home

126 Previous work suggests that glucose transporters are major mediators of arsenic impo

127 sidue in trans-membrane domain 7 of class II glucose transporters as a determinant of fructose transp

128 asite can counteract genetic ablation of its glucose transporter by increasing the flux of glutamine-

129 docytic regulation of the Hxt6 high affinity glucose transporter by showing that Snf1 interacts speci

130 this work, we demonstrated the regulation of glucose transporters by hypoxia inducible factor-1alpha

131 and localization of the major fatty acid and glucose transporters, CD36 (cluster of differentiation 3

132 at multiple levels to trigger high-affinity glucose transporter endocytosis.

133 6-phosphatase activity but increased Slc2a2 glucose transporter expression in corticosterone-treated

134 In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively

135 T5 is a fructose-specific transporter in the glucose transporter family (GLUT, SLC2 gene family).

136 c trafficking rate of the GLUT4 facilitative glucose transporter from intracellular stores to the pla

137 The glucose transporter from Staphylococcus epidermidis, Glc

138 rt by up-regulating the transcription of the glucose transporter genes GLUT-1 and GLUT-3.

139 chromatin accessibility for two neighboring glucose transporter genes in response to changes in gluc

140 Along with upregulation of the glucose transporter, glucose transporter 1, and glycolyt

141 Overexpressing human glucose transporter GLUT-3 in motor neurons mitigates TD

142 ke by selectively targeting and upregulating glucose transporters GLUT-1 and GLUT-3.

143 osing to depression (insulin receptors Insr, glucose transporters Glut-4 and Glut-12, and the regulat

144 M1 polarization involves upregulation of the glucose transporter (GLUT) GLUT1 to facilitate increased

145 We report an insulin-facilitated glucose transporter (Glut) inhibitor conjugate, in which

146 We hypothesized that glucose transporter (GLUT) protein, member 5 (GLUT5) is

147 trate that HFD feeding of mice downregulates glucose transporter (GLUT)-1 expression in blood-brain b

148 sufficient expression levels of facilitative glucose transporter (GLUT)1 in up to 50% of all patients

149 tose-transporting member of the facilitative glucose transporter (GLUT, SLC2) family, is a therapeuti

150 d (P = 0.026) placental mRNA expression of a glucose transporter (GLUT-3) and increased (P = 0.037) p

151 cific for glucose and a homolog of the human glucose transporters (GLUT, SLC2 family).

152 Dysfunction of the cerebral glucose transporter GLUT1 (encoded by SLC2A1) is known t

153 e created a murine model of myeloid-specific glucose transporter GLUT1 (Slc2a1) deletion.

154 The facilitated glucose transporter GLUT1 (SLC2A1) is an important media

155 omplex mTORC1 induces both expression of the glucose transporter Glut1 and aerobic glycolysis for Tef

156 ORC1) signaling, decreased expression of the glucose transporter Glut1 and hexokinase 2, and reduced

157 Expression of the glucose transporter Glut1 and of glycolytic enzymes as w

158 ) type 1 E. coli activated expression of the glucose transporter GLUT1 and repressed expression of th

159 elated genes increased and the nonintestinal glucose transporter GLUT1 appeared at the basolateral me

160 The glucose transporter GLUT1 at the blood-brain barrier (BB

161 ng activation, with proportionally increased glucose transporter Glut1 expression and mitochondrial m

162 nflammation, reduces sulfenylation of SIRT6, glucose transporter Glut1 expression, glucose uptake, an

163 F also reduced oligodendrocyte expression of glucose transporter GLUT1 induced by NMDAR activity.

164 s, apparently by increasing translocation of glucose transporter GLUT1 to the plasma membrane.

165 In contrast to the glucose transporter GLUT1, GLUT3 was regulated by enviro

166 5) show that PKC directly phosphorylates the glucose transporter Glut1, in order to promote glucose u

167 of oligodendroglial NMDA receptors mobilizes glucose transporter GLUT1, leading to its incorporation

168 BSG1 binds to the glucose transporter GLUT1, resulting in increased glucos

169 layer and glucose transport activity via the glucose transporter GLUT1.

170 ound that Ffar1 suppresses expression of the glucose transporter Glut1.

171 nsporter LAT1 and enhanced expression of the glucose transporter GLUT1.

172 by promoting cell surface expression of the glucose transporter GLUT1/Slc2a1.

173 Glucose transporters GLUT1 (transports glucose) and GLUT

174 olerance, it increased the expression of the glucose transporters GLUT1 and -4 in the muscle and enha

175 Expression of the glucose transporter (GLUT1) in oligodendrocytes was asse

176 at the deletion of only one highly expressed glucose transporter, Glut1 or Glut3, in cancer cells doe

177 the phosphorylation of the erythrocyte/brain glucose transporter, GLUT1, without a clear understandin

178 Indeed, the glucose transporter GLUT2 is located at the basolateral,

179 actor HIF1alpha, lactate dehydrogenase LDH5, glucose transporter GLUT2, phosphorylated pyruvate dehyd

180 ron of SLC2A2, which encodes the facilitated glucose transporter GLUT2, was associated with a 0.17% (

181 millimolar glucose in rat mucus; we detected glucose transporter GLUT3 in rat and toad (Caudiverbera

182 f the gene SLC2A3-which encodes the neuronal glucose transporter GLUT3-could modulate AO in HD.

183 ls (BTICs) co-opt the neuronal high affinity glucose transporter, GLUT3, to withstand metabolic stres

184 tion based on addiction to the high-affinity glucose transporter, Glut3.

185 Defects in translocation of the glucose transporter GLUT4 are associated with peripheral

186 Glycogen and glucose transporter GLUT4 are decreased.

187 ial (AP) firing, nerve terminals rely on the glucose transporter GLUT4 as a glycolytic regulatory sys

188 The surfacing of the glucose transporter GLUT4 driven by insulin receptor act

189 The glucose transporter GLUT4 facilitates insulin-stimulated

190 stimuli converge on the translocation of the glucose transporter GLUT4 from intracellular vesicles to

191 controls exocytosis of the insulin-sensitive glucose transporter Glut4 in adipocytes.

192 d muscle cells to sequester the facilitative glucose transporter GLUT4 in an intracellular compartmen

193 r membrane traffic of the insulin-responsive glucose transporter GLUT4 in humans.

194 duces translocation of the insulin-regulated glucose transporter GLUT4 to the plasma membrane, where

195 Although astrocytes appear to express glucose transporter GLUT4, glucose entry across the astr

196 C1D4, and lower muscle protein levels of the glucose transporter GLUT4, with increasing number of p.A

197 endent increase in glucose transport through glucose transporter GLUT4- and PI3K-dependent mechanisms

198 ss, insulin receptors and insulin-responsive glucose transporters (Glut4) often colocalize in neurons

199 s Profiles databases, we discovered that the glucose transporter GLUT6 is highly upregulated in LPS-a

200 orters in the body, the passive facilitative glucose transporters (GLUTs) and the secondary active so

201 FDG is only a good substrate for facilitated-glucose transporters (GLUTs) but not for sodium-dependen

202 n cell membranes is mediated by facilitative glucose transporters (GLUTs) embedded in lipid bilayers.

203 te (NMDA) subtype and resulted in removal of glucose transporters (GLUTs) from the surfaces of dendri

204 lucose transporters (SGLTs) and facilitative glucose transporters (GLUTs) in glucose homeostasis was

205 ship between the distribution of MAN-LIP and glucose transporters (GLUTs) on the cells.

206 FDG is a good substrate only for facilitated-glucose transporters (GLUTs), not for sodium-dependent g

207 sporters have been characterized, namely the glucose transporters (GLUTs), sodium-glucose symporters

208 through the cellular membrane by a family of glucose transporters (GLUTs).

209 is mainly imported into cells by facilitated glucose transporters (GLUTs).

210 aive T cells by regulating the expression of glucose transporters, glycolytic enzymes, and metabolic

211 ermore, the mRNA levels of the HIF-1 targets glucose transporters, glycolytic enzymes, and pyruvate d

212 ortant for both flagellar trafficking of the glucose transporter GT1 and for successful cytokinesis a

213 Two structural models of the class II glucose transporters, hSLC2A9 and hSLC2A5, based on the

214 of either of two low-affinity, high-capacity glucose transporters, Hxt1 and Hxt3, suppresses the 2DG

215 or induction of expression of genes encoding glucose transporters (HXTs).

216 Mice overexpressing the Glut4 glucose transporter in adipocytes have elevated lipogene

217 GLUT1 is the main glucose transporter in ECs and becomes uncoupled from gl

218 a markedly elevated expression of the GLUT1 glucose transporter in lung SqCC, which augments glucose

219 nd plasma membrane localization of the GLUT4 glucose transporter in skeletal muscle, but are not defi

220 rogression is associated with a reduction in glucose transporters in both neurons and endothelial cel

221 results demonstrate the requirement for two glucose transporters in lung adenocarcinoma, the dual bl

222 There are two major classes of glucose transporters in the body, the passive facilitati

223 lytic metabolism; however, the role of other glucose transporters in this process is largely unknown.

224 SLC45A1 thus represents the second cerebral glucose transporter, in addition to GLUT1, to be involve

225 0Val]) in SLC45A1, encoding another cerebral glucose transporter, in two consanguineous multiplex fam

226 tions and upon treatment with the hepatocyte glucose transporter inhibitor trehalose.

227 dification of alpha-arrestins, which promote glucose transporter internalization and degradation, cau

228 Transplacental glucose transport by glucose transporter isoform 1 (GLUT-1) on the syncytiotr

229 GLUT1 (glucose transporter isoform 1/Slc2a1) is highly expresse

230 eading to an increase in insulin-independent glucose transporter levels, enhanced cellular glucose up

231 In Leishmania mexicana parasites, a unique glucose transporter, LmxGT1, is selectively targeted to

232 HxtB was confirmed to be a low affinity glucose transporter, localizing to the plasma membrane u

233 enantiomer, its cellular entry is not mainly glucose transporter-mediated.

234 opportunities to transpass the BBB/BBTB via glucose-transporter-mediated transcytosis by MA.

235 Glucose transporters mediating glucose entry are key pro

236 nown as solute carrier family 2, facilitated glucose transporter member 1.

237 Facilitated glucose transporter member 14 (GLUT14), encoded by the s

238 Overexpressing IP3 receptor or glucose transporter mitigates the S1RE102Q-induced eye p

239 ange did not render the human protein into a glucose transporter, molecular dynamics simulations reve

240 The abundance of cell surface glucose transporters must be precisely regulated to ensu

241 ndent signals on chromosome 17 in SLC5A10, a glucose transporter not previously known to transport 1,

242 GLUT1 (SLC2A1) is the primary rate-limiting glucose transporter on proinflammatory-polarized MPhis.

243 erivative-modified insulin (Glc-Insulin) and glucose transporters on erythrocytes (or red blood cells

244 re we show that its orthologue, the vacuolar glucose transporter OsSWEET2b from rice (Oryza sativa),

245 The expression of glucose transporters, oxidative metabolism, and mitochon

246 s overexpression of GLUT4, the high capacity glucose transporter, partially rescues viral replication

247 Glucose transporters play an essential role in cancer ce

248 opic peptide (GIP), forskolin) that act upon glucose transporters, potassium and calcium channels, an

249 imited human renal sodium gradient-dependent glucose transporter protein (SGLT2) mRNA and protein exp

250 and that of GLUT 2 and the sodium-dependent glucose transporter protein 1 (SGLT1), was not regulated

251 ion of argininosuccinate synthase (ASS1) and glucose transporter protein type 1 (GLUT1).

252 egulation of argininosuccinate synthase- and glucose transporter protein type 1-mediated arginolysis

253 Overall, the PEP-PTS glucose transporter PtsG appears to play important roles

254 cific phenolic inhibitors of SGLT1 and GLUT2 glucose transporters, reduced the glucose transport of a

255 We further show that inhibitors of glucose transporters selectively kill SLC7A11(high) canc

256 ntended to target tumor cells overexpressing glucose transporters selectively.

257 is study was to determine whether the sodium-glucose transporter SGLT1 in the ventromedial hypothalam

258 protein expression of HIF-1alpha and of the glucose transporters SGLT1, SGLT2, and GLUT1.

259 ficient mice with an inhibitor of the kidney glucose transporter SGLT2 to lower their blood level of

260 tered glucose load through the Na(+)-coupled glucose transporter SGLT2, and specific inhibitors of SG

261 C5A2, the gene encoding the sodium-dependent glucose transporter (SGLT2), a protein targeted pharmaco

262 The importance of sodium-coupled glucose transporters (SGLTs) and facilitative glucose tr

263 glucose import system, the sodium-dependent glucose transporters (SGLTs), in pancreatic and prostate

264 UTs) and the secondary active sodium-coupled glucose transporters (SGLTs).

265 eased AHR binding in the gene regions of the glucose transporter, SLC2A1, and the glycolytic enzyme,

266 mammalian mechanosensory protein; GLUT1, the glucose transporter; SLC4A1, the anion transporter; RhAG

267 ciated with reduced intestinal expression of glucose transporters (sodium-dependent glucose transport

268 ty, we show that genetic overexpression of a glucose transporter, specifically in neurons, rescues li

269 ow the physical phase of the membrane alters glucose transporter structural dynamics using molecular-

270 of potent, orally bioavailable inhibitors of glucose transporters, targeting both GLUT1 and GLUT3.

271 In contrast, S-acylation of GLUT4, a glucose transporter that extensively co-localises with I

272 ch stimulates the translocation of the GLUT4 glucose transporter to cell membranes.

273 nsulin-stimulated translocation of the GLUT4 glucose transporter to the plasma membrane (PM) of adipo

274 intracellular vesicles containing the GLUT4 glucose transporter to the plasma membrane.

275 Therefore, targeting glucose transporters to regulate aerobic glycolysis is a

276 n causes the exocytic translocation of GLUT4 glucose transporters to stimulate glucose uptake in fat

277 ge neutral amino acid transporter 1 (LAT-1), glucose transporter type 1 (Glut-1), and permeability-gl

278 Glucose transporter type 1 (GLUT1) deficiency syndrome (

279 Hepatic SCD1 deficiency enhanced glucose transporter type 1 (GLUT1) expression in the liv

280 ells with high xCT expression and identified glucose transporter type 1 (GLUT1).

281 ularly document unique or unusual aspects of glucose transporter type 1 deficiency (G1D).

282 sess its therapeutic effect in patients with glucose transporter type 1 deficiency syndrome (GLUT1-DS

283 PA increased the amount of glucose transporter type 1-positive cerebral blood vesse

284 eleasing factor, pro-opiomelanocortin B, and glucose transporter type 2 in distinct brain regions of

285 se into Xenopus oocytes expressing the human glucose transporter type 2.

286 Overexpression of glucose transporter type 3 (GLUT3) in nonmalignant human

287 changes in the expression or localization of glucose transporter type 3.

288 osity as a result of persistent cell surface glucose transporter type 4 (GLUT4) in adipocytes resulti

289 The discovery of the insulin-responsive glucose transporter type 4 (GLUT4) protein in 1988 inspi

290 ormyltransferase/IMP cyclohydrolase-mediated glucose transporter type 4 (GLUT4) translocation.

291 d reduced ( approximately 31%) the levels of glucose transporter type 4 (GLUT4) without affecting the

292 as confirmed by increased mRNA expression of glucose transporter type 4 (GLUT4), lipoprotein lipase (

293 has been proposed to function in delivery of glucose transporter type 4 (GLUT4)-containing vesicles t

294 6 (cluster of differentiation 36) and GLUT4 (glucose transporter type 4), are also unchanged.

295 Glucose transporter type I deficiency (G1D) is commonly

296 sion of proteins involved in glucose uptake (glucose transporters types 1 and 3 [GLUT-1 and -3, respe

297 in luminal expression of Sglt1, a key renal glucose transporter, uncovering a novel regulatory pathw

298 A surprising finding was that a subset of glucose transporters was among the most downregulated pr

299 A mutant lacking all seven major glucose transporters was highly resistant to arsenic, an

300 80s, when GLUT4, the major insulin-regulated glucose transporter, was identified, my lab observed tha