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+/- mice have epileptiform discharges on electroen

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

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

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

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

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

9 GLUTs have been identified as rate-limiting in specific

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

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

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

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

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

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

16 downstream proteins, glucose transporter 1 (GLUT-1), erythropoietin (EPO), and vascular endothelial

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

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

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

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

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

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

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

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

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

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

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

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

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

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

31 ns in adiponectin and glucose transporter 4 (GLUT 4) and increases in dipeptidylpeptidase 4, suppress

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

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

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

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

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

45 underscore the importance of dual GLUT-1 and GLUT-3 inhibition to efficiently suppress tumor cell gro

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

47 upregulating glucose transporters GLUT-1 and GLUT-3.

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

49 of the glucose transporter genes GLUT-1 and GLUT-3.

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

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

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

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

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

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

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

57 prevented down-regulation of adiponectin and GLUT 4 and increases in SOCS3 levels in a TNF-alpha-indu

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 all intestinal sugar transporters, SGLT1 and GLUTs (GLUT1, 2 and 5).

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

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

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

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

70 Unlike other bacterial GLUT homologs (for example, XylE), GlcP(Se) has a loose

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

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

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

74 lete picture of glucose utilization via both GLUT and SGLT transporters in health and disease stages.

75 lete picture of glucose utilization via both GLUT and SGLT transporters in health and disease states.

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

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

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

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 r findings underscore the importance of dual GLUT-1 and GLUT-3 inhibition to efficiently suppress tum

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

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

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

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

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

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

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

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

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

97 -25% identity with other murine facilitative GLUTs.

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

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

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

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

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

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

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

105 8]-fluoro-d-glucose (2-FDG), a substrate for GLUTs.

106 d blood-brain barrier gene expression (e.g., GLUT-1), CD31, and tight junction protein ZO1 expression

107 rocytic HIF-1alpha, and the downstream genes GLUT-1, EPO, and VEGF-A (p < 0.05), in the absence of a

108 anscription of the glucose transporter genes GLUT-1 and GLUT-3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Oocytes injected to express small intestinal GLUTs were inhibited by teas, but SGLT1 was not.

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

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

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

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

135 Most GLUTs and their bacterial counterparts differ in the tra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 = 0.0003) correlated with gene expression of GLUT-4.

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

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

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

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

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

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

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

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

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

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

165 with characteristics consistant with that of GLUT-1.

166 g studies for functional characterization of GLUTs in BC.

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

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

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

170 r glucose uptake and increased expression of GLUTs.

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

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

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

174 s used to determine cellular localization of GLUTs.

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

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

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

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

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

180 change in placental cross-sectional area or GLUT 1 expression, prepregnant HF feeding significantly

181 n activity and expression of SGLT1 and other GLUTs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 represents a novel, second insulin-sensitive GLUT.

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

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

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

204 f specific hypothalamic neurons (AgRP or SFO(GLUT)) restored cue-evoked food- or water-seeking, InsCt

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

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

207 Myeloid-restricted deletion of Slc2a1 (GLUT-1) or pharmacological inhibition of S100A8/A9 reduc

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

209 A could thus be a new chemical tool to study GLUT function and a promising lead for developing antica

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

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

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

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

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

215 The GLUT (SLC2) family of membrane-associated transporters a

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

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

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

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

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

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

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

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

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

225 Thus, the GLUT-mediated in vivo glucose utilization measured by 2-

226 Thus, the GLUT-mediated in vivo glucose utilization measured by 2-

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

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

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

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

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

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

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

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

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

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

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

238 Overexpressing human glucose transporter GLUT-3 in motor neurons mitigates TDP-43 dependent defec

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

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

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

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

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

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

245 ves upregulation of the glucose transporter (GLUT) GLUT1 to facilitate increased glucose uptake and g

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

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

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

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

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

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

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

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

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

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

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

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

258 al mRNA expression of a glucose transporter (GLUT-3) and increased (P = 0.037) placental IGF-2 mRNA e

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

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

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

262 geting and upregulating glucose transporters GLUT-1 and GLUT-3.

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

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

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

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

267 a homolog of the human glucose transporters (GLUT, SLC2 family).

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

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

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

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

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

273 strate for facilitated-glucose transporters (GLUTs) but not for sodium-dependent glucose co-transport

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

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

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

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

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

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

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

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

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

283 e only for facilitated-glucose transporters (GLUTs), not for sodium-dependent glucose cotransporters

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

285 protein expression of glucose transporters (GLUTs).

286 embrane by a family of glucose transporters (GLUTs).

287 o cells by facilitated glucose transporters (GLUTs).

288 sible were facilitated glucose transporters (GLUTs).

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

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

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

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

293 eveals important differences between the two GLUT homologs.

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

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