ライフサイエンスコーパス: GLUT

1 GLUT 3 demonstrated a polarized distribution limited to

2 GLUT-1 expression in the basal plasma membrane also corr

3 GLUT-1 is also present in an intracellular storage pool

4 GLUT-1+/- mice have epileptiform discharges on electroen

5 GLUT-1, found in high density at the BBB appears to main

6 GLUT-1, whose sequence was originally deduced from cDNAs

7 GLUT-2 differs from other members of the facilitated glu

8 GLUT-2 expression in beta cells of Zucker diabetic fatty

9 GLUT-2 protein rose 17-fold in AdCMV-OB-Rb-treated ZDF i

10 GLUT-5 is not incorporated into the lateral plasma membr

11 GLUTs have been identified as rate-limiting in specific

12 transport by glucose transporter isoform 1 (GLUT-1) on the syncytiotrophoblast microvillous and basa

13 determine the role of glucose transporter 1 (GLUT-1) and GLUT-3 in L-14C-DHA transport and to evaluat

14 12 by using the terms glucose transporter 1 (GLUT-1) deficiency syndrome, glucose transporter defect,

15 led that, for HTLV-1, glucose transporter 1 (GLUT-1) functions at a postbinding step during HTLV-3 En

16 hat overexpression of glucose transporter 1 (GLUT-1) in mesangial cells could induce a "diabetic cell

17 amma (PPAR-gamma) and glucose transporter 1 (GLUT-1) levels in human brain microvascular endothelial

18 tes and expression of glucose transporter 1 (GLUT-1), taurine transporter (TAUT), sodium-dependent ne

19 MA), D2-40, CD34, and glucose transporter 1 (GLUT-1).

20 ntly attached to anti-glucose transporter-1 (GLUT-1) antibodies via carbodiimide chemistry.

21 lines have shown that glucose transporter-1 (GLUT-1) can function as a receptor for human T-cell leuk

22 ysiologic hypoxia and glucose transporter-1 (GLUT-1) expression.

23 in the expression were observed for GLUT-1, GLUT-3, and MCT-4.

24 glycolysis, including expressions of GLUT-1, GLUT-3, PFK, LDH, phosphorylated AMPK activity and HIF-1

25 In neoplastic skin, HIF-1alpha, GLUT-1, and PGK-1 mRNAs localized in the basal and immed

26 Immediately after wounding, HIF-1alpha, GLUT-1, and PGK-1 mRNAs were detectable in basal keratin

27 In epidermal carcinogenesis, HIF-1alpha, GLUT-1, PGK-1, and VEGF mRNAs were just detectable in ea

28 Neither HIF-1alpha, GLUT-1, PGK-1, nor VEGF mRNA was detectable in unwounded

29 ose transporter 1 and glucose transporter 3 (GLUT-1 and GLUT-3), phosphofructokinase (PFK), lactate d

30 The facilitative glucose transporter-3 (GLUT 3) and hexokinase I were examined in postnatal mous

31 uptake (glucose transporters types 1 and 3 [GLUT-1 and -3, respectively]), phosphorylation (hexokina

32 ulin receptor (InsR), glucose transporter-4 (GLUT-4) and type 1 insulin-like growth factor receptor (

33 otubes by stimulating glucose transporter-4 (GLUT-4) membraned translocation.

34 where a similar modest effect on hnRNP L (a GLUT-1 and VEGF 3'-untranslated region-binding protein),

35 CREB and Sp3 also interacted to bring about GLUT 3 expression in response to development/cell differ

36 To assess additional GLUTs, immunoblots were performed.

37 n of several adipogenic genes (LpL, adipsin, GLUT-4, aP2, beta3-adrenergic receptor, and peroxisome p

38 ct brain GLUT 1 mRNA and protein, it altered GLUT 3 mRNA levels in a region-specific manner, with a t

39 Our results suggest that, although GLUT-5 may be involved in the control of electromotility

40 GLUT-4 (15 +/- 2% to 30 +/- 3%, P < .02) and GLUT-1 (41 +/- 4% to 58 +/- 3%, P < .03) compared with t

41 nd brain cellular distribution of GLUT 1 and GLUT 3 expression.

42 Both GLUT 1 and GLUT 3 mRNA levels demonstrated a similar developmental

43 t and hypoxic-ischemia upon brain GLUT 1 and GLUT 3 mRNA levels.

44 In the brain, both GLUT 1 and GLUT 3 were noted in neuron- and glial-enriched cultures

45 xpression of UCP-2 and UCP-3, and GLUT-1 and GLUT-2 and significantly decreased plasma norepinephrine

46 rter 1 and glucose transporter 3 (GLUT-1 and GLUT-3), phosphofructokinase (PFK), lactate dehydrogenas

47 ion for the glucose transporters, GLUT-1 and GLUT-3.

48 These results indicate that both GLUT-1 and GLUT-4 are important in ischemia-mediated myocardial glu

49 dial glucose transporter content (GLUT-1 and GLUT-4 by immunoblotting), and functional recovery from

50 nce of MGUp on gene expression of GLUT-1 and GLUT-4 was characterized by multiple-regression analysis

51 nd protein expression analysis of GLUT-1 and GLUT-4.

52 e role of glucose transporter 1 (GLUT-1) and GLUT-3 in L-14C-DHA transport and to evaluate the effect

53 press detectable levels of HSPGs, NRP-1, and GLUT-1.

54 ich coincided with an increase in GLUT-2 and GLUT-10 abundance.

55 ivity and expression of UCP-2 and UCP-3, and GLUT-1 and GLUT-2 and significantly decreased plasma nor

56 m in vivo and the distribution of GLUT-4 and GLUT-1 by use of immunoblotting of sarcolemma and intrac

57 demonstrated the presence of both GLUT-4 and GLUT-1 on cardiac myocytes.

58 assayed include Oct3, Rex1, Nanog, Cdx2 and GLUT-1.

59 cumulation mediated predominantly by DHA and GLUT transporters, 6-bromo-6-deoxy-L-ascorbic acid accum

60 s the vascular endothelial growth factor and GLUT-1 genes.

61 Thus, inhibition of PPAR-gamma and GLUT-1 by E. coli K1 is a novel pathogenic mechanism in

62 The suppression of PPAR-gamma and GLUT-1 by the bacteria in the brain microvessels of newb

63 armacological upregulation of PPAR-gamma and GLUT-1 levels may provide novel therapeutic avenues.

64 Here, the roles of HSPGs and GLUT-1 in HTLV-1 and HTLV-2 Env-mediated binding and ent

65 d-glucose (4-FDG), a substrate for SGLTs and GLUTs; and 2-deoxy-2-[F-18]-fluoro-d-glucose (2-FDG), a

66 ere incubated initially with GNR tagged anti-GLUT-1 antibodies and then with a fluorescent-tagged sec

67 paracellular glucose flux, as well as apical GLUT-mediated glucose uptake.

68 e and lipid metabolism-related genes such as GLUT-1, and chemotaxis and recruitment genes such as CCL

69 cose (glucose analog), but not when blocking GLUT.

70 Both GLUT 1 and GLUT 3 mRNA levels demonstrated a similar dev

71 In the brain, both GLUT 1 and GLUT 3 were noted in neuron- and glial-enrich

72 n increase in the sarcolemma content of both GLUT-4 (15 +/- 2% to 30 +/- 3%, P < .02) and GLUT-1 (41

73 uorescence demonstrated the presence of both GLUT-4 and GLUT-1 on cardiac myocytes.

74 These results indicate that both GLUT-1 and GLUT-4 are important in ischemia-mediated myo

75 -ischemia did not significantly affect brain GLUT 1 mRNA and protein, it altered GLUT 3 mRNA levels i

76 eperfusion injury cause an increase in brain GLUT 3 expression, as a response to synaptogenesis and s

77 development and hypoxic-ischemia upon brain GLUT 1 and GLUT 3 mRNA levels.

78 rted efficiently by native GLUT-2 but not by GLUT-1.

79 evelop in part by exclusion of DHA uptake by GLUT transporters when blood glucose levels rise above n

80 how the transport of dehydroascorbic acid by GLUTs is a means by which tumors acquire vitamin C and i

81 noside (Me4FDG), which is not transported by GLUTs; and (iii) measurement of in vivo SGLT activity in

82 xic induction of HIF-1 target genes (CDKN1A, GLUT-1, and VEGF), tumor angiogenesis in vitro, cell mig

83 uman, dog, and sheep, and 69% to the chicken GLUT 3 peptides.

84 ce), myocardial glucose transporter content (GLUT-1 and GLUT-4 by immunoblotting), and functional rec

85 Studies defining GLUTs as being rate-limiting in specific tumor contexts,

86 as normal lymphocytes to uncover deregulated GLUT family members in myeloma.

87 rse transcriptase-PCR as follows: VEGF, EPO, GLUT-1, adrenomedullin, propyl 4-hydroxylase alpha, MT-1

88 Some genes, for example GLUT-1, MT-1, CELF, MKP-1, and t-PA did not show any hyp

89 superfamily (MFS) transporters (for example, GLUTs and SUTs).

90 lls, the primary target of HTLV-2, expressed GLUT-1 at dramatically higher levels than CD4(+) T cells

91 The human vessels expressed GLUT-1 and merosin, immunodiagnostic markers for infanti

92 thalamic glucose sensing protein expression (GLUTs, glucokinase) were measured.

93 ntified member of the mammalian facilitative GLUT superfamily that exhibits approximately 20-25% iden

94 The facilitative GLUT inhibitor cytochalasin B, but not the sodium-depend

95 sensitive to the levels of the facilitative GLUT protein GLUT4.

96 -25% identity with other murine facilitative GLUTs.

97 s the basolateral membrane via facilitative, GLUT-mediated, transport.

98 ian facilitative glucose transporter family (GLUT), we refer to the protein as GLUT10 (HGMW-approved

99 ansporter in the glucose transporter family (GLUT, SLC2 gene family).

100 is constancy occurs because there are so few GLUTs on the sarcolemma surface in the basal state and t

101 RECENT FINDINGS: GLUTs, enabling the facilitative entry of glucose into a

102 ferences in the expression were observed for GLUT-1, GLUT-3, and MCT-4.

103 ough cancer-specific expression patterns for GLUTs are being identified, comprehensive analyses subst

104 8]-fluoro-d-glucose (2-FDG), a substrate for GLUTs.

105 tion of cardiac glucose transporters (GLUTs; GLUT-4) and reduces lactate production.

106 sms are used to replace GLUT1, the normal HF GLUT, with GLUT4, the major glucose transporter in adipo

107 associated with physiologic hypoxia and high GLUT-1 expression.

108 in the absence of physiologic hypoxia, high GLUT-1 expression, by itself, was insufficient to ensure

109 ulation and were severely hypoxic, with high GLUT-1 expression.

110 egulatory components of glucose homeostasis (GLUT-4, G6PDH, Hk-2 and Gly-Syn-1).

111 idermidis, GlcPSe, is a homolog of the human GLUT sugar transporters of the major facilitator superfa

112 value of 28+/-1.6 muM phloretin for class I GLUT proteins and a concentration of 40+/-0.6 muM phlore

113 n was unaltered; however, HS increased ileal GLUT-2 protein expression (P=0.06).

114 ata indicate that active site differences in GLUT members could be exploited to further enhance ligan

115 uptake, which coincided with an increase in GLUT-2 and GLUT-10 abundance.

116 Increased GLUT-1, hexokinase II, and phospho-AMPK protein in muscl

117 tress-activated Cn is critical for increased GLUT 4 and IGF1R expression and activation.

118 y showed no effect on the sodium independent GLUT family of glucose transporters, and the most potent

119 The ability to target individual GLUT isoforms in an acute and reversible manner provides

120 nalyses substantiating a role for individual GLUTs are still required.

121 o investigate the contribution of individual GLUTs to health and disease and to develop targeted trea

122 c expression of GLUT1, -2, -4, or -9 induced GLUT isoform-specific ER transport activity in HEK293T c

123 dynamic stimulus on glomerular cells induces GLUT-1 overexpression followed by greater glucose uptake

124 In TB, InsR, GLUT-4 and IGF-1R mRNA levels were greater in L group fe

125 CM and FPCM (but not 2D) preserved insulin, GLUT-2, and PDX-1 mRNA expression.

126 and were not significantly hypoxic, with low GLUT-1 expression.

127 blood-brain barrier (BBB) phenotype marker, GLUT-1, suggesting that in brain the angiogenic role of

128 enous CREB concentrations, and CREB mediated GLUT 3 transcription.

129 obesity reduced cardiac glucose metabolism, GLUT, and AMP-activated protein kinase (AMPK) levels, an

130 the promoter and exon 1 regions of the mouse GLUT-1 gene.

131 A significantly reversed the reduced muscle GLUT-4 translocation and the increased liver phosphoenol

132 at of native GLUT-1 (3.7 +/- 0.4) and native GLUT-2 (26.3 +/- 3.3).

133 which are transported efficiently by native GLUT-2 but not by GLUT-1.

134 that was intermediate between that of native GLUT-1 (3.7 +/- 0.4) and native GLUT-2 (26.3 +/- 3.3).

135 no change in Km for 2-DOG relative to native GLUT-2 but exhibited a significant reduction in capacity

136 ed as completely specific for SVCTs, but not GLUTs, and provide a new strategy to determine the contr

137 Our work reveals critical roles for novel GLUT family members and highlights a therapeutic strateg

138 t for the decline in suprachiasmatic nuclear GLUT 3 immunoreactivity.

139 GLUT-2 with the N-terminal 87 amino acids of GLUT-1 exhibited no change in Km for 2-DOG relative to n

140 ts allowed us to elucidate the activation of GLUT by plasma membrane phospholipids and to extend the

141 for gene and protein expression analysis of GLUT-1 and GLUT-4.

142 (1) A chimera consisting of GLUT-1 with the C-terminal tail of GLUT-2 had a Km for 2

143 (2) A chimera consisting of GLUT-2 with the N-terminal 87 amino acids of GLUT-1 exhi

144 To determine the contribution of GLUT blockade to protease inhibitor-mediated glucose dys

145 e findings in the context of determinants of GLUT oligomeric structure and transport function.

146 he tissue and brain cellular distribution of GLUT 1 and GLUT 3 expression.

147 n general, while the spatial distribution of GLUT 3 and hexokinase I did not change with age, a tempo

148 e metabolism in vivo and the distribution of GLUT-4 and GLUT-1 by use of immunoblotting of sarcolemma

149 The multiple duplications of GLUT genes suggest that the GLUT family probably emerged

150 In contrast, MVM protein expression of GLUT 3 or SNAT4 was unaltered.

151 The dependence of MGUp on gene expression of GLUT-1 and GLUT-4 was characterized by multiple-regressi

152 ed to the postulation that the expression of GLUT-1 could be upregulated in glomeruli that are expose

153 MVM protein expression of GLUT-1, TAUT, SNAT-2 and LAT-1/2 was reduced in MNR.

154 phocytes with TGF-beta induced expression of GLUT-1, which has recently been reported to function as

155 a diminished MGUp result, gene expression of GLUT-4 was significantly (P = 0.004) lower in ZDF rats.

156 = 0.0003) correlated with gene expression of GLUT-4.

157 erebral glycolysis, including expressions of GLUT-1, GLUT-3, PFK, LDH, phosphorylated AMPK activity a

158 ubstrate specificity and kinetic function of GLUT-2, recombinant adenoviruses were used to express na

159 tion studies revealed that overexpression of GLUT-1 in CD4(+) T cells increased HTLV-2 entry, while e

160 F-beta1 in turn, maintains overexpression of GLUT-1, perpetuating a signaling sequence that has, as i

161 ciple regarding the therapeutic potential of GLUT-targeted compounds, we include evidence of the anti

162 In addition, we include the regulation of GLUT 2, which facilitates the final step in the transpor

163 trient homeostasis, whereas up-regulation of GLUT-2 and GK is leptin-independent, requiring only high

164 rated for the first time the pivotal role of GLUT-1, TMEM16F, and SDF4 in angiogenesis.

165 revealed that in addition to segregation of GLUT-1 (luminal>abluminal), the intracellular enzyme hex

166 ction via a reduction in AMPK stimulation of GLUT-4 translocation, revealing a mechanism of metabolic

167 isting of GLUT-1 with the C-terminal tail of GLUT-2 had a Km for 2-DOG of 9.9 +/- 1.5 that was interm

168 s 7, 8, and 12 whose expression, and that of GLUT 2 and the sodium-dependent glucose transporter prot

169 with characteristics consistant with that of GLUT-1.

170 The in vitro translation of GLUT-1 mRNA of diabetic rats (0.793 +/- 0.047 arbitrary

171 g studies for functional characterization of GLUTs in BC.

172 Two classes of GLUTs are identified in chondrocytes, constitutively exp

173 MGUp against gene and protein expression of GLUTs in the diabetic heart of an animal model of type 2

174 hromatosis, also had increased expression of GLUTs, HDACs, and DNMTs.

175 r glucose uptake and increased expression of GLUTs.

176 Inhibition of GLUTs by using cytochalasin B indicated that infected ce

177 WZB117 inhibition of GLUTs expressed in HEK293 cells follows the order of pot

178 Cell surface labeling of GLUTs indicated that RabGAP deficiency impairs retention

179 s used to determine cellular localization of GLUTs.

180 aphy, in mice aiming to evaluate the role of GLUTs and SGLTs in controlling glucose distribution and

181 d to be those that appear to be dependent on GLUT transport of DHA rather than sodium-dependent AA up

182 microscopic tumors but had little effect on GLUT-1 expression.

183 ll type that relies exclusively or mainly on GLUT for co-transport of glucose and DHA including neuro

184 mportance of detailed biochemical studies on GLUT protein expression levels in combination with PET i

185 ression of cerebral glucose transporter one (GLUT-1) and whether there are age-related differences in

186 GLUT1 mRNA was the only GLUT isoform expressed in control cells and in cells exp

187 ation of glucose transporter (GLUT)-4 and/or GLUT-1 to the sarcolemma in vivo is unknown.

188 n activity and expression of SGLT1 and other GLUTs.

189 ulus-secretion pathway including PC1/3, PC2, GLUT-1, glucokinase, and K-ATP channel complex (Sur1 and

190 ol) but did not affect AMPK phosphorylation, GLUT-4 translocation and glucose uptake.

191 ared with the distributions of pimonidazole, GLUT-1 expression, bromodeoxyuridine, and Hoechst 33342

192 sizes (lobules) consisting of CD34-postive, GLUT-1-negative endothelial cells and SMA-positive peric

193 oli, XylEEc, the other prominent prokaryotic GLUT homolog, GlcPSe, is equipped with a conserved proto

194 ve substrates of glucose transport proteins (GLUTs) and possess hypoxia-selective radiosensitization

195 The derived rabbit GLUT 3 peptide revealed 84% homology to the mouse, 82% t

196 ve cloned and sequenced a full length rabbit GLUT 1 and partial rabbit GLUT 3 cDNAs.

197 The tissue-specific expression of rabbit GLUT 3 mimics that of the human closely.

198 full length rabbit GLUT 1 and partial rabbit GLUT 3 cDNAs.

199 We conclude, that the rabbit GLUT 3 peptide sequence exhibits 82-84% homology to that

200 alpha) and retinoid X receptor, up-regulated GLUT-2 expression in islets of normal rats, but not in Z

201 nt mice was due to decreased levels of renal GLUT 2 (rGLUT2) but not sodium-glucose cotransporter 2 a

202 halamic expression of the insulin-responsive GLUT 4, but not glucokinase, was reduced by 30% in NIRKO

203 Based on the RNAi results, GLUT-1 mediated, at least in part, the uptake of DHA, wh

204 s on histone 3, reduced TNF-alpha secretion, GLUT-1 upregulation, and increased glucose uptake.

205 s a therapeutic strategy entailing selective GLUT inhibition to specifically target aberrant glucose

206 UT12 may represent another insulin-sensitive GLUT, transgenic (TG) mice that overexpress GLUT12 were

207 represents a novel, second insulin-sensitive GLUT.

208 However, several GLUT-independent mechanisms have been postulated.

209 he hypoxia-dependent upregulation of several GLUTs provides a rational basis to develop these glucoaz

210 nohistochemistry, we determined that several GLUTs (GLUT2, GLUT4, GLUT8, and GLUT9), a sodium-glucose

211 The relative expression of DC-SIGN, GLUT-1, HSPGs, and NRP-1 first was examined on both DCs

212 However, significant GLUT-4 surface labeling was found in the ischemic region

213 Similarly, GLUT-4 translocation was significantly reduced in NTG (7

214 entification and targeting of tumor-specific GLUTs provide a promising approach to block glucose-regu

215 pression of PPARgamma2, fatty acid synthase, GLUT-4, and leptin both in control and prenylation inhib

216 We found that GLUT-1 expression in the microvillous plasma membrane of

217 In conclusion, we demonstrate that GLUTs are sufficient for mediating ER glucose transport

218 d overload-induced uptake demonstrating that GLUTs mediate this effect.

219 We show that GLUTs are most significant for glucose uptake into the b

220 The GLUT-1 concentration in insulin-treated diabetic group w

221 The GLUT-1 mass in cerebral microvessels was reduced in diab

222 The GLUT-1 mRNA content of cerebral tissue in diabetic rats

223 The GLUT-1+/- murine phenotype mimics the classical human pr

224 lutions, the animals were sacrificed and the GLUT-4 analysed by western blot.

225 embrane domains, a hallmark structure of the GLUT family.

226 The facilitative sugar transporters of the GLUT type can transport the oxidized form of the vitamin

227 We report the expression of the GLUT-1 3'-untranslated region RNA-binding protein, heter

228 eterozygous mutations or hemizygosity of the GLUT-1 gene cause Glut-1 DS.

229 nse mutations resulting in truncation of the GLUT-1 protein.

230 In contrast to the effect of the GLUT-2 C terminus on Km for 2-DOG, this substitution did

231 port is incorporated by using a model of the GLUT-2 glucose transporter.

232 duplications of GLUT genes suggest that the GLUT family probably emerged by gene duplications and mu

233 Sp3, CREB, and MSY-1 binding to the GLUT 3 DNA was confirmed by the chromatin immunoprecipit

234 The involvement of the GLUTs in vitamin C uptake by the xenografted tumors was

235 d activity, the lipid-induced effects on the GLUTs remain poorly understood.

236 MFS transporters for their relevance to the GLUTs by comparing conservation of functionally critical

237 ogs of the human D-glucose transporters, the GLUTs (SLC2), provide information about the structure of

238 ence that chondrocytes transport DHA via the GLUTs and that this transport mechanism is modestly sele

239 eeded to better understand the role of these GLUTs in fructose-induced diseases.

240 This GLUT-1+/- mouse model creates an opportunity to investig

241 le GLUT 1 mRNA was observed in most tissues, GLUT 3 was expressed predominantly in the brain, placent

242 cose uptake in L6 myotubes was attributed to GLUT 4 translocation, the most downstream factor in the

243 e showed greater efficiency in translocating GLUT-4 to the PM and of increasing glucose capture by sk

244 ate translocation of the glucose transporter GLUT-4 to the PM of animal skeletal muscle.

245 increased expression of glucose transporter (GLUT) 1 mRNA and protein, and GLUT9 mRNA.

246 Insulin stimulates glucose transporter (GLUT) 4 vesicle translocation from intracellular storage

247 of glucose mediated by glucose transporter (GLUT) 4, which is expressed mainly in skeletal muscle, h

248 ecular underpinnings of glucose transporter (GLUT) activation in cancer, knowledge that could facilit

249 rations on facilitative glucose transporter (GLUT) expression in rat mesangial cells.

250 Glucose transporter (GLUT) expression, activity and translocation represent c

251 evelop a novel class of glucose transporter (GLUT) inhibitors.

252 tly at the level of the glucose transporter (GLUT) protein in cells derived from both peripheral and

253 We hypothesized that glucose transporter (GLUT) protein, member 5 (GLUT5) is the primary fructose

254 g of mice downregulates glucose transporter (GLUT)-1 expression in blood-brain barrier (BBB) vascular

255 Expression of glucose transporter (GLUT)-1 in retinas and cultured cells was determined by

256 or distribution of the glucose transporter (GLUT)-1 in the RPE and retina of the Bsg(-/-) mouse.

257 scription factor HIF-1, glucose transporter (GLUT)-1, phosphoglycerate kinase (PGK)-1, and vascular e

258 to the translocation of glucose transporter (GLUT)-4 and/or GLUT-1 to the sarcolemma in vivo is unkno

259 a trend towards reduced glucose transporter (GLUT)-4 mRNAs when compared with pups fed a balanced cho

260 via phloretin-sensitive glucose transporter (GLUT)-mediated uptake, which coincided with an increase

261 levels of facilitative glucose transporter (GLUT)1 in up to 50% of all patients.

262 insulin stimulation of glucose transporter (GLUT)4 translocation requires at least two distinct insu

263 ber of the facilitative glucose transporter (GLUT, SLC2) family, is a therapeutic target for diabetes

264 Recently, a glucose transporter, GLUT-1, heparan sulfate proteoglycans (HSPGs), and neuro

265 The high-Km glucose transporter, GLUT-2, and the high-Km hexokinase of beta cells, glucok

266 A sugar transporter, GLUT-5, was proposed based on its localization in the OH

267 at of candidate apical fructose transporters GLUTs 7, 8, and 12 whose expression, and that of GLUT 2

268 showed the presence of glucose transporters (GLUT) 1, 4, and 8.

269 DHA), enters cells via glucose transporters (GLUT) and is then converted back to AA within these cell

270 titium by facilitative glucose transporters (GLUT).

271 ing proteins (UCP) and glucose transporters (GLUT).

272 The glucose transporters (GLUT/SLC2A) are members of the major facilitator superfa

273 iew will highlight key glucose transporters (GLUTs) and current therapies targeting this class of pro

274 if taste cells express glucose transporters (GLUTs) and metabolic sensors that serve as sugar sensors

275 r, the contribution of glucose transporters (GLUTs) and the mechanisms regulating subsequent glucose

276 e passive facilitative glucose transporters (GLUTs) and the secondary active sodium-coupled glucose t

277 diated by facilitative glucose transporters (GLUTs) embedded in lipid bilayers.

278 resulted in removal of glucose transporters (GLUTs) from the surfaces of dendritic processes in hippo

279 GLTs) and facilitative glucose transporters (GLUTs) in glucose homeostasis was studied in mice using

280 rough the facilitative glucose transporters (GLUTs) in the form of dehydroascorbic acid, which is the

281 hibitors acutely block glucose transporters (GLUTs) in vitro, and this may contribute to altered gluc

282 ibution of MAN-LIP and glucose transporters (GLUTs) on the cells.

283 mediated by a group of glucose transporters (GLUTs) on the plasma membrane.

284 that insulin-sensitive glucose transporters (GLUTs) other than GLUT4 may exist.

285 Glucose transporters (GLUTs) were monitored by 3-O-methyl-D-glucose uptake.

286 racterized, namely the glucose transporters (GLUTs), sodium-glucose symporters (SGLTs), and SWEETs.

287 protein expression of glucose transporters (GLUTs).

288 o cells by facilitated glucose transporters (GLUTs).

289 sible were facilitated glucose transporters (GLUTs).

290 age, we tested whether glucose transporters (GLUTs, SGLTs) destined for the plasma membrane are activ

291 anslocation of cardiac glucose transporters (GLUTs; GLUT-4) and reduces lactate production.

292 RNA expression for the glucose transporters, GLUT-1 and GLUT-3.

293 transcripts for the following transporters: GLUT-1; MCT 1 and 2; OAT1; Oatp1; mdr 1a and 1b; MRP 1 a

294 eveals important differences between the two GLUT homologs.

295 chiasmatic nucleus and the cerebellum, where GLUT 3 expression was limited to neuronal cell somata.

296 at least in part, the uptake of DHA, whereas GLUT-3 had a minimal effect on DHA transport.

297 ens with or without intervillositis, whereas GLUT-1 expression in the basal plasma membrane was lowes

298 To assess which GLUT, hexose competition experiments were performed.

299 While GLUT 1 mRNA was observed in most tissues, GLUT 3 was exp

300 Studies with GLUTs expressed in and solubilized from HEK cells show t