ライフサイエンスコーパス: GLUT3

1 des the high-affinity glucose transporter 3 (GLUT3).

2 ucose transporters, targeting both GLUT1 and GLUT3.

3 6-bromo-6-deoxy-L-ascorbic acid, by GLUT1 or GLUT3.

4 mino-acid protein that is 94.5% identical to GLUT3.

5 T3 and likely resulted from a duplication of GLUT3.

6 stis is about four times higher than that of GLUT3.

7 of the neuron specific glucose transporter, GLUT3.

8 ressing glucose transporter isoform GLUT1 or GLUT3.

9 s, relative to the other isoforms, GLUT1 and GLUT3.

10 ugh an increase in the cellular synthesis of GLUT3.

11 n, to the neuronal glucose transport protein GLUT3.

12 erved in the 3'-UTR of both canine and human Glut3.

13 ulated GLUT4 >> GLUT1 approximately neuronal GLUT3.

14 t in liposomes containing purified GLUT4 and GLUT3.

15 m resolution crystal structure of SA47-bound GLUT3.

16 to induce T1DM in concert with induction of GLUT3.

17 ha-regulated neuronal transporter of glucose GLUT3.

18 on to the high-affinity glucose transporter, Glut3.

19 4) but did not correlate with p27, BCL-2, or GLUT3.

20 lative abundance of the Glut1 (4.5-fold) and Glut3 (3.5-fold) proteins as determined by Western blot

21 t differential expression in the placenta of Glut3, a glucose transporter essential for normal embryo

22 rotein- coding gene in the bithorax complex, Glut3, a sugar-transporter homolog, can be deleted witho

23 for activity-dependent increases in surface GLUT3 after stimulation of the NMDARs.

24 These differences in the C-termini of Glut3 among the species may result in kinetic or mechani

25 Tamoxifen increased cerebral cortical Glut3 and 4 mRNA levels, but did not affect Glut1, IGF1,

26 vels and lesser but significant increases in Glut3 and 4 protein levels.

27 M9 are 4-fold more catalytically active than GLUT3 and GLUT1 containing GLUT3 TM9.

28 ssibility exists whereby other Gluts such as Glut3 and Glut4 may also support the influx of glucose i

29 atment induced two- to fourfold increases in Glut3 and Glut4 mRNA levels and lesser but significant i

30 gA is a potent inhibitor of GLUT1 as well as GLUT3 and GLUT4, with an IC(50) value of low nanomolar f

31 Glut3 and Glut6 are expressed in glial cells and neural

32 GLUT3 and GLUT8 mRNA are constitutively expressed in cho

33 ed in chondrocytes, constitutively expressed GLUT3 and GLUT8, and the inducible GLUT1 and GLUT9.

34 th a genomic organization similar to that of GLUT3 and likely resulted from a duplication of GLUT3.

35 GLUT3 and OCT4 expression were correlated suggesting tha

36 were significantly overexpressed, including GLUT3 and REA (overexpressed in all GCTs) and CCND2 and

37 ly associated with the expression of HK2 and Glut3 and shown to be dependent on Akt signaling by both

38 In LHA, IIH increased GLUT3 and SUR1 gene expression to an equal extent, with

39 ways to probe the pathophysiological role of GLUT3 and tackle GLUT3-dependent cancers.

40 human, mouse and rat glucose transporter 3 (Glut3), and found to be 88.3, 84.9 and 84.3% identical,

41 nsporters present in skeletal muscle, GLUT1, GLUT3, and GLUT11.

42 to evaluate the relevant transporters GLUT1, GLUT3, and GLUT4 and vitamin C transporters SVCT1 and SV

43 3)C-DHA via the glucose transporters (GLUT1, GLUT3, and GLUT4) in TRAMP tumor.

44 three different glucose transporters, GLUT1, GLUT3, and GLUT4, and the transferrin receptor.

45 Hexokinase-I, GLUT3, and lactate dehydrogenase-A and -B were ubiquitou

46 IIH decreased MCT2, GLUT3, and SUR1 gene profiles in the VMH; CV4 lactate in

47 BTICs preferentially express Glut3, and targeting Glut3 inhibits BTIC growth and tumo

48 nal glucose transporter 3-encoding sequences(Glut3) available for the purposes of alignment studies.

49 ossing LV-GLUT1/bEND.3 cell monolayers or LV-GLUT3/ bEND.3 cell monolayers, of which GLUT1 and GLUT3

50 ycle revealed a significant surge in ovarian Glut3 (but not Glut1) expression at the time of ovulatio

51 pression as well as translation of Glut1 and Glut3 (but not of Gluts 2, 4, or 5).

52 ocampal AMPA GluR1 subunits and the neuronal GluT3, but decreased expression of hippocampal brain-der

53 Glut3, but not Glut1, correlates with poor survival in b

54 Silencing GLUT3 caused a reduction in glucose uptake and lactate p

55 GLUT1 and GLUT3 cDNA were further verified by polymerase chain rea

56 s necessary for optimal association of GLUT1-GLUT3 chimeras with parental GLUT1 in HEK cells.

57 Cell surface GLUT1 and GLUT3 containing GLUT1 TM9 are 4-fold more catalytically

58 Glut3-containing vesicles co-purify with "classical" syn

59 Unlike classical synaptic vesicles, Glut3-containing vesicles possess a high level of aminop

60 s study, we found that the promoter of human GLUT3 contains three potential cAMP response element (CR

61 , suggesting that HNE protein conjugation of GLUT3 contributes to decreases in neuronal glucose utili

62 ich encodes the neuronal glucose transporter GLUT3-could modulate AO in HD.

63 pathophysiological role of GLUT3 and tackle GLUT3-dependent cancers.

64 Expressed mutant constructs of GLUT1 and GLUT3 did not transport DHA.

65 GLUT1 and GLUT3 display allosteric transport behavior.

66 GLUT1 and the neuronal glucose transporter GLUT3 do not form heterocomplexes in human embryonic kid

67 LUT1 domains are substituted with equivalent GLUT3 domains and vice versa, we show that GLUT1 transme

68 contrast, platelets isolated from GLUT1 and GLUT3 double-knockout (DKO) mice, which lack the ability

69 ls that the overexpression of GLUT1, but not GLUT3, enriches for genes involved in glycolysis, mitoch

70 These were tested for in vivo inhibition of GLUT3 expressed in hexose transporter-deficient yeast ce

71 roteolyses CREB, resulting in a reduction of GLUT3 expression and consequently impairing glucose upta

72 nNOS-phosphomimetic mutant (S1412D) enhanced GLUT3 expression at cell surface.

73 Consistently, silencing Glut3 expression diminishes the protective effect of mic

74 unoblots were not affected by the diminished Glut3 expression in the Glut3(+/-) mice.

75 Thus, we compared levels of GLUT1 and GLUT3 expression in the retina, cerebrum, and their resp

76 after M1 polarization stimuli and found that GLUT3 expression increased after M2 stimulation in macro

77 Northern (RNA) analysis showed that GLUT3 expression increased during infection.

78 dies and the most proximal dendrites, unlike GLUT3 expression that is observed throughout the neuropi

79 essed by transcriptomics and costaining, and GLUT3 expression was significantly decreased in nonheali

80 ents with atopic dermatitis showed increased GLUT3 expression, and a calcipotriol-induced model of at

81 as a site of cyclically determined Glut1 and Glut3 expression, and disclose the ability of IL-1 to in

82 nfection and apoptosis, as well as increased GLUT3 expression, consistent with increased neuronal met

83 icroRNA-7, by down-regulating RelA, augments Glut3 expression, promotes glycolysis, and subsequently

84 ndent protein kinase significantly increased GLUT3 expression.

85 ted CREB, which had less activity to promote GLUT3 expression.

86 and CRE3 were required for the promotion of GLUT3 expression.

87 tes a PAK4-YAP/TAZ signaling axis to enhance Glut3 expression.

88 infection matched the sequence for the human GLUT3 facilitative glucose transporter, a high-velocity-

89 The Glut3(-/-) genotype is intrauterine lethal by 7days post

90 the sugar transporters SGLT1, GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5.

91 qPCR was used to measure MCT2, GLUT3, GLUT4, GK, and SUR1 transcripts in the microdisse

92 IIH alone did not alter mean DVC MCT2, GLUT3, GLUT4, GK, or SUR1 mRNA levels, but these transcr

93 Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivef

94 hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glu

95 GLUT4 membrane trafficking, while enhancing GLUT3 glycosylation and neuronal glucose uptake.

96 ncreased brain glucose transporters, Glut1 & Glut3, greater brain derived neurotrophic factor (BDNF),

97 ptake of glucose into the mouse brain, since Glut3 haploinsufficiency does not impair brain glucose u

98 A mouse line with a null allele for Glut3 has been developed.

99 The facilitative GLUT1 and GLUT3 hexose transporters are expressed abundantly in ma

100 Both the GLUT1 and GLUT3 high-affinity, facilitative glucose transporters w

101 GLUT3 immunoprecipitated from hippocampal membranes of d

102 hat this correlated with increased levels of GLUT3 in HD patient cells.

103 M2-like macrophages expressed GLUT3 in human wound tissues as assessed by transcriptom

104 In contrast to the expression of GLUT3 in many tissues, both isoforms of GLUT14 are speci

105 n rat mucus; we detected glucose transporter GLUT3 in rat and toad (Caudiverbera caudiverbera) OSN ci

106 he non-homogeneous distribution of GLUT1 and GLUT3 in the brain.

107 without GLUT3, suggesting broader roles for GLUT3 in the regulation of endocytosis.

108 t of vitamin C, was transported by GLUT1 and GLUT3 in Xenopus laevis oocytes with transport rates sim

109 Upon expression of GLUT1 or GLUT3 in Xenopus oocytes, BrDHA was neither transported

110 verexpression of glucose transporter type 3 (GLUT3) in nonmalignant human breast cells activated know

111 ghly expressed glucose transporter, Glut1 or Glut3, in cancer cells does not impair tumor growth, whe

112 ion of the glucose transporters Glut1 and/or Glut3, in either the incipient pre-skeletal mesenchyme w

113 (G3iA, IC(50) ~ 7 uM) was most selective for GLUT3, inhibiting less strongly only GLUT2 (IC(50) ~ 29

114 ty for GLUT1-5 revealed that the most potent GLUT3 inhibitor (G3iA, IC(50) ~ 7 uM) was most selective

115 We identify an exofacial GLUT3 inhibitor SA47 and elucidate its mode of action by

116 None of the GLUT3 inhibitors affected GLUT5, three inhibited GLUT1 w

117 GLUT3 inhibitors can provide new ways to probe the patho

118 multiple myeloma's reliance on GLUT4, these GLUT3 inhibitors may discriminately hinder glucose entry

119 -deficient yeast cells, resulting in six new GLUT3 inhibitors.

120 preferentially express Glut3, and targeting Glut3 inhibits BTIC growth and tumorigenic potential.

121 GLUT3 interacted directly with GTP-bound RAS in vitro an

122 GLUT3 is a high-affinity glucose transporter primarily r

123 Although Glut3 is a known driver of a cancer stem cell phenotype,

124 rain and cultured neuroendocrine PC12 cells, Glut3 is localized at the cell surface and, also, in a d

125 We conclude that a 50% decrease in Glut3 is not limiting for the uptake of glucose into the

126 Thus, GLUT3 is required for efficient alternative macrophage p

127 We, therefore, conclude that Glut3 is targeted to secretory vesicles in both neurons

128 GLUT3 is the glucose transporter responsible for maintai

129 euronal activity controls glucose influx via GLUT3 is unknown.

130 However, what leads to the decreased GLUT3 is yet unknown.

131 Neuronal glucose transporter 3 (GLUT3) is decreased in AD brain and correlates with tau

132 Glucose transporter 3 (GLUT3) is the main facilitative glucose transporter in n

133 expression of GLUTs, particularly GLUT1 and GLUT3, is required to fuel the hyperproliferation of can

134 These studies suggest GLUT1 and GLUT3 isoforms are the specific glucose transporter isof

135 tic activity increased surface expression of GLUT3 leading to an elevation of intracellular glucose.

136 GLUT3 levels were greater in cerebral gray matter than i

137 by 7days post-coitis, but the heterozygous (Glut3(+/-)) littermate survives, exhibiting rapid post-n

138 se in Glut3(+/-) mice was not different from Glut3(+/+) littermates, despite 50% less Glut3 protein e

139 oxy glucose was similarly not different from Glut3(+/-) littermates in the total amount, time course,

140 nalyses of tumors demonstrate that Glut1 and Glut3 loss decreases glucose uptake, which is mainly dep

141 ction assays in N2A neuroblasts using murine GLUT3-luciferase reporter constructs mapped enhancer act

142 Conditional deletion of Glut3 (LysM-Cre Glut3fl/fl) impaired M2 polarization of

143 (a marker for cell proliferation), GLUT1 and GLUT3 (markers for glucose transportation), p53 and p27

144 The conservation in the UTR suggests that Glut3 may be post-transcriptionally regulated.

145 uced motor coordination improvements through GLUT3-mediated metabolic rebalancing.

146 tail vein-injected ((3))H-2-deoxy glucose in Glut3(+/-) mice was not different from Glut3(+/+) litter

147 ed by the diminished Glut3 expression in the Glut3(+/-) mice.

148 amount, time course, or brain imaging in the Glut3(+/-) mice.

149 K1, PFK1, glucose transporter 1 (GLUT1), and GLUT3 mRNA expression.

150 hanced the expression of the gene coding for GLUT3 mRNA.

151 CBP does not interact with the C terminus of GLUT3 or GLUT4.

152 associated with expression of GLUT1 but not GLUT3 or GLUT5.

153 overexpression of the Glut1, but not Glut2, Glut3, or Glut4, glucose transporter.

154 -LIP was significantly improved by GLUT1 and GLUT3 overexpression cells.

155 Given the prevalence of GLUT1 and GLUT3 overexpression in many cancers and multiple myelom

156 tion of critical glycolytic genes, including GLUT3, PFKP, and PKM.

157 GLUT3 promoted IL-4/STAT6 signaling, independently of it

158 omoted luciferase expression driven by human GLUT3-promoter.

159 rom Glut3(+/+) littermates, despite 50% less Glut3 protein expression in the brain.

160 Flow cytometry showed that GLUT3 protein expression increased specifically in the H

161 ion, increases in HNE protein conjugation of GLUT3 provide a potential mechanism for stress- and diab

162 way of purified human glucose transporter 3 (GLUT3) reconstituted within synthetic lipid bilayers.

163 Glut3 was aligned with the comparable human glut3 region and was shown to be 70% identical over a re

164 NMDAR-induced increase in surface GLUT3 represents a novel pathway for control of energy s

165 - and 10-nm Stokes radius particles, whereas GLUT3 resolves as a 6-nm particle.

166 hydrophilic transmembrane helices, thrusting GLUT3's microstate sampling toward folded structures.

167 The canine Glut3 sequence also exhibits 74.5% aa identity with a no

168 tituted membrane helix 9 with the equivalent GLUT3 sequence.

169 .5% aa identity with a non-mammalian chicken Glut3 sequence.

170 finity neuronal glucose transporter, type 3 (Glut3, SLC2A3).

171 sustains HPC energy homeostasis via GLUT4-to-GLUT3 substrate switching, positioning 18F-FDG PET as a

172 macropinocytosis were also impaired without GLUT3, suggesting broader roles for GLUT3 in the regulat

173 ted the influence of synaptic stimulation on GLUT3 surface expression and glucose import in primary c

174 kt inhibitor I (Akt-I) blocked NMDAR-induced GLUT3 surface expression while a nNOS-phosphomimetic mut

175 We report here a 2355-bp sequence of canine Glut3 that encodes a deduced protein of 496 amino acids

176 tablish IL-1 as the first known regulator of Glut3, the most efficient Glut known to date.

177 Substitution of GLUT1 TM9 with GLUT3 TM9 causes chimeric GLUT1 to resolve as a mixture

178 Substitution of GLUT3 TM9 with GLUT1 TM9 causes chimeric GLUT3 to resolv

179 cally active than GLUT3 and GLUT1 containing GLUT3 TM9.

180 of GLUT3 TM9 with GLUT1 TM9 causes chimeric GLUT3 to resolve as 6- and 10-nm Stokes radius particles

181 neuronal high affinity glucose transporter, GLUT3, to withstand metabolic stress.

182 dependent nNOS phosphorylation is coupled to GLUT3 trafficking.

183 The ability of IL-1 to upregulate Glut1 and Glut3 transcripts proved time-, dose-, nitric oxide-, an

184 rease in the neuronal glucose transporter 3 (Glut3), underlies this glycolysis-promoting effect.

185 cations, we report here the engineering of a GLUT3 variant, designated GLUT3exo, that can be probed f

186 e apparent Km of DHA transport via GLUT1 and GLUT3 was 1.1 +/- 0.2 and 1.7 +/- 0.3 mM, respectively.

187 indicated that the transcytosis by GLUT1 and GLUT3 was a pathway of MAN-LIP into brain, and the speci

188 f the 5'-untranslated region (UTR) of canine Glut3 was aligned with the comparable human glut3 region

189 Importantly, human brain GLUT3 was correlated with full-length CREB positively an

190 r ovary cells overexpressing either GLUT1 or GLUT3 was increased 2-8-fold over control cells.

191 DHA transport activity in both GLUT1 and GLUT3 was inhibited by 2-deoxyglucose, D-glucose, and 3-

192 Unlike plasma membrane-localized GLUT1, GLUT3 was localized primarily to endosomes and was requi

193 n contrast to the glucose transporter GLUT1, GLUT3 was regulated by environmental oxygen and localise

194 GLUT3 was unchanged.

195 nsport carried out by glucose transporter 3 (GLUT3) was downregulated in TKI-sensitive LAD cells.

196 nst the inward- and outward-facing models of GLUT3, we selected ~ 200 ligand candidates.

197 / bEND.3 cell monolayers, of which GLUT1 and GLUT3 were overexpressed.

198 se (cGK) increased the surface expression of GLUT3, which was repressed by Rp-8-pCPT-cGMPS, a potent

199 ome 12p13.3 (17.1M), about 10 Mb upstream of GLUT3, with which it shares remarkable identity.