ライフサイエンスコーパス: glucose transporter

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

2 vity, demonstrating that Hxs1 functions as a glucose transporter.

3 ohydrate metabolism including GLUT1, a major glucose transporter.

4 or of the ptsG mRNA, which encodes the major glucose transporter.

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

6 This effect is mediated by the Glut4 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 e by preventing plasma membrane targeting of glucose transporters.

11 g step of its utilization, is facilitated by glucose transporters.

12 searched until July 2012 by using the terms glucose transporter 1 (GLUT-1) deficiency syndrome, gluc

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

14 s in placental homogenates and expression of glucose transporter 1 (GLUT-1), taurine transporter (TAU

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

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

17 Glucose transporter 1 (GLUT1) immunohistochemistry was p

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

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

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

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

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

23 absorbed into intestine cells via the sodium glucose transporter 1 (SGLT-1) and glucose transporter 2

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

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

26 Immunohistochemical Ki-67 and glucose transporter 1 analysis was used to evaluate tumo

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

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

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

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

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

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

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

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

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

36 2 and the cerebrovascular-selective proteins glucose transporter 1, permeability-glycoprotein, and la

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

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

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

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

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

42 synthesized and covalently attached to anti-glucose transporter-1 (GLUT-1) antibodies via carbodiimi

43 The expression of glucose transporter-1 (Glut-1), hexokinase-1 and -2 (Hk-

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

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

46 a proliferative arteriopathy associated with glucose transporter-1 (Glut1) up-regulation and a glycol

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

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

49 rom the small intestine via sodium-dependent glucose transporter-1 and glucose transporter-2, which m

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

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

52 at cells in the invasive edges expressed the glucose transporter-1 and the sodium-hydrogen exchanger-

53 to meet its increased bioenergetic demands; glucose transporter-1 is up-regulated, basolateral gluco

54 ally included perturbed vascular endothelial glucose transporter-1 localization.

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

56 s vascular endothelial growth factor (VEGF), glucose transporter-1, and pyruvate dehydrogenase kinase

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

58 atients, duodenal levels of sodium-dependent glucose transporter-1, glucose transporter-2, and T1R2 t

59 ligation and puncture mice sodium-dependent glucose transporter-1, glucose transporter-2, and T1R2 t

60 man) and relative levels of sodium-dependent glucose transporter-1, glucose transporter-2, and taste

61 etabolism and increases the transcription of Glucose-transporter-1 mRNA, and of Hexokinase and Pyruva

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

63 Here we assessed the impact of glucose transporter 2 (Glut2) gene inactivation in adult

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

65 ntiation markers villin, sucrase-isomaltase, glucose transporter 2 (GLUT2), and dipeptidyl peptidase

66 he sodium glucose transporter 1 (SGLT-1) and glucose transporter 2 (GLUT2); various peptides and horm

67 on of HCMV-induced glucose transporter 4 and glucose transporter 2 expression, leading to inhibition

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

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

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

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

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

73 s of sodium-dependent glucose transporter-1, glucose transporter-2, and T1R2 transcript were reduced

74 mice sodium-dependent glucose transporter-1, glucose transporter-2, and T1R2 transcripts were reduced

75 s of sodium-dependent glucose transporter-1, glucose transporter-2, and taste receptor type 1 member

76 a sodium-dependent glucose transporter-1 and glucose transporter-2, which may both be regulated by in

77 Neuronal glucose transporter 3 (GLUT3) is decreased in AD brain a

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

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

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

81 , Akt, and AS160, to promote the net gain of glucose transporter 4 (GLUT4) at the plasma membrane of

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

83 Mice that over-express glucose transporter 4 (Glut4) in skeletal muscle, heart,

84 Insulin stimulates the mobilization of glucose transporter 4 (GLUT4) storage vesicles to the pl

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

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

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

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

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

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

91 ng a ubiquitin regulatory X (UBX) domain for glucose transporter 4 (GLUT4)).

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

93 d cells results in reduction of HCMV-induced glucose transporter 4 and glucose transporter 2 expressi

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

95 dation, and plasma membrane translocation of glucose transporter 4.

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

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

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

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

100 tilization at the mRNA and protein level and glucose transporter-4 (GLUT4) localization in skeletal m

101 In adipocytes, vesicles containing glucose transporter-4 (GLUT4) redistribute from intracel

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

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

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

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

106 herapy, pulmonary failure, immunodeficiency, glucose transporter aberrations, insulin-resistant diabe

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

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

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

110 lts demonstrate that Hxs1 is a high-affinity glucose transporter and required for fungal virulence.

111 cose that is taken up by macrophages through glucose transporters and because mannose receptors are e

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

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

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

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

116 rface membrane proteins: GLUT1 (the red cell glucose transporter) and then GLUT2 and GLUT4, the red c

117 increased by 50% the surface localization of glucose transporter, and enhanced by 25% cellular glucos

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

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

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

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

122 Glucose transporters are central players in glucose home

123 Glucose transporters are required to bring glucose into

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

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

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

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

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

129 transporter 1 (GLUT-1) deficiency syndrome, glucose transporter defect, and SLC2A1-gene.

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

131 family 2, member 2 (also known as GLUT2), a glucose transporter expressed in the liver, is one ribos

132 ible nitric oxide synthase, endothelin1, and glucose transporter expression in cerebral microvessels

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 SLC2A10/GLUT10, a member of the facilitative glucose transporter family, are associated with altered

137 liberates intracellularly sequestered GLUT4 glucose transporters for translocation to the cell surfa

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

139 The glucose transporter from Staphylococcus epidermidis, Glc

140 s, insulin causes the translocation of GLUT4 glucose transporters from intracellular vesicles to the

141 ania mexicana encompasses a cluster of three glucose transporter genes designated LmxGT1, LmxGT2 and

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

143 s by regulating delivery of the facilitative glucose transporter, glucose transporter isoform 4 (GLUT

144 s reduces the level of plasma membrane-bound glucose transporter, glucose uptake, and the consequent

145 infection, as inactivation of the bacterial glucose transporter gluP reduced both intracellular surv

146 mponents could modulate translocation of the glucose transporter GLUT-4 to the PM of animal skeletal

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

148 nactive analogue to develop a novel class of glucose transporter (GLUT) inhibitors.

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

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

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

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

153 f mitochondria uncoupling proteins (UCP) and glucose transporters (GLUT).

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

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

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

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

158 s glucose uptake directly, by binding to the glucose transporter GLUT1 and inducing GLUT1 internaliza

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

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

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

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

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

164 as critical, as transgenic expression of the glucose transporter Glut1 rescued cytokine production of

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

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

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

168 roblasts, triggering increased expression of glucose transporter GLUT1, lactate production, and extru

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

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

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

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

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

174 g/dL and led to decreased gene expression of glucose transporter GLUT1.

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

176 Glucose transporters GLUT1 (transports glucose) and GLUT

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

178 ransport of hyperpolarized (13)C-DHA via the glucose transporters (GLUT1, GLUT3, and GLUT4) in TRAMP

179 Moreover, the levels of the glucose transporter, GLUT1, are also reduced compared to

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

181 In addition increased brain glucose transporters, Glut1 & Glut3, greater brain deriv

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

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

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

185 ession, we investigated whether facilitative glucose transporters GLUT2 and GLUT5-12 transported DHA.

186 GLUT1 and the neuronal glucose transporter GLUT3 do not form heterocomplexes in

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

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

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

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

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

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

193 The glucose transporter GLUT4 facilitates insulin-stimulated

194 regulated by reversible translocation of the glucose transporter GLUT4 from intracellular stores to t

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

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

197 tes with insulin results in insertion of the glucose transporter GLUT4 into the plasma membrane and s

198 The glucose transporter GLUT4 plays a central role in mainta

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

200 ) reduced concentration of insulin-regulated glucose transporter GLUT4, and (iii) changed feedback fr

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

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

203 muscle is mediated by the major facilitative glucose transporter Glut4.

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

205 oncomitantly, the sarcolemmal content of the glucose transporter, GLUT4, increased by 90% during isch

206 nterparts, we found that upregulation of the glucose transporter GLUT6 was more closely associated wi

207 This review will highlight key glucose transporters (GLUTs) and current therapies targe

208 However, the contribution of glucose transporters (GLUTs) and the mechanisms regulati

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

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

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

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

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

214 Glucose transporters (GLUTs) were monitored by 3-O-methy

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

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

217 he transporters responsible were facilitated glucose transporters (GLUTs).

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

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

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

221 Expression of several glucose transporter (HXT) genes in yeast is repressed by

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

223 s cerevisiae expresses different isoforms of glucose transporters (HXTs) in response to different lev

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

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

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

227 de production, and increased expression of a glucose transporter in PD-L1-deficient hosts.

228 e glycogen reserves and of concentrating the glucose transporter in the plasma membrane (PM).

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

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

231 red firing rates with a plausible density of glucose transporters in the nodal membrane, without the

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

233 e regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS and matched contr

234 0Val]) in SLC45A1, encoding another cerebral glucose transporter, in two consanguineous multiplex fam

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

236 The LmxGT1 glucose transporter is selectively targeted to the flage

237 lucose/H(+) symporter is homologous to human glucose transporters, is very specific and has high avid

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

239 ery of the facilitative glucose transporter, glucose transporter isoform 4 (GLUT4), to the plasma mem

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

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

242 The GLUT4 facilitative glucose transporter mediates insulin-dependent glucose u

243 Glucose transporters mediating glucose entry are key pro

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

245 ansport (solute carrier family 2 facilitated glucose transporter, member 2 (SLC2A2) and solute carrie

246 SLC2A1 (solute carrier family 2 [facilitated glucose transporter] member 1) showed association with N

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

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

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

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

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

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

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

254 , vascular endothelial growth factor (VEGF), glucose transporter protein 1 (Glut-1), and hypoxia-indu

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

256 CD34 expression) and for markers of hypoxia (glucose transporter protein 1 [Glut-1] and pimonidazole)

257 04), and between flow-extraction product and glucose transporter protein expression (r = -0.50, P = .

258 correlated negatively with pimonidazole and glucose transporter protein expression, indicating the p

259 sensitive to the levels of the facilitative glucose transporter protein, GLUT4.

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

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

262 ntended to target tumor cells overexpressing glucose transporters selectively.

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

264 st a clear decrease in the expression of the glucose transporters SGLT1 and SGLT2 under hypoxic condi

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

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

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

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

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

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

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

272 gulator of the high-affinity, Na(+)-coupled, glucose transporter sodium-dependent glucose cotransport

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

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

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

276 lta T cells express higher surface levels of glucose transporters than alphabeta T cells and, when ac

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

278 ococcus epidermidus, homologs of the human D-glucose transporters, the GLUTs (SLC2), provide informat

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

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

281 Fatty acid and glucose transporters translocate between the sarcolemma

282 Glucose transporter type 1 (GLUT1) deficiency syndrome (

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

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

285 maltase (SI); dipeptidyl peptidase 4 (Dpp4); glucose transporter type 2 (Glut2); and villin were meas

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

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

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

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

290 nse by (18)F-FDG PET and objective response, glucose transporter type 4 (GLUT4) expression, and KIT/P

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

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

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

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

295 receptor levels ( approximately 2-fold) and glucose transporter type 4 (GLUT4; approximately 1.3-fol

296 6 (cluster of differentiation 36) and GLUT4 (glucose transporter type 4), are also unchanged.

297 Glucose transporter type I deficiency (G1D) is commonly

298 take by co-opting the high affinity neuronal glucose transporter, type 3 (Glut3, SLC2A3).

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

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