ライフサイエンスコーパス: GLUT3

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

2 T3 and likely resulted from a duplication of GLUT3.

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

4 of the neuron specific glucose transporter, GLUT3.

5 ressing glucose transporter isoform GLUT1 or GLUT3.

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

7 ugh an increase in the cellular synthesis of GLUT3.

8 n, to the neuronal glucose transport protein GLUT3.

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

10 ha-regulated neuronal transporter of glucose GLUT3.

11 ulated GLUT4 >> GLUT1 approximately neuronal GLUT3.

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

13 t in liposomes containing purified GLUT4 and GLUT3.

14 6-bromo-6-deoxy-L-ascorbic acid, by GLUT1 or GLUT3.

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

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

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

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

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

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

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

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

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

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

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

26 Glut3 and Glut6 are expressed in glial cells and neural

27 GLUT3 and GLUT8 mRNA are constitutively expressed in cho

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

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

30 GLUT3 and OCT4 expression were correlated suggesting tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 GLUT1 and GLUT3 display allosteric transport behavior.

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

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

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

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

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

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

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

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

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

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

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

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

71 ndent protein kinase significantly increased GLUT3 expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

85 GLUT3 immunoprecipitated from hippocampal membranes of d

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

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

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

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

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

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

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

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

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

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

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

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

98 GLUT3 is the glucose transporter responsible for maintai

99 euronal activity controls glucose influx via GLUT3 is unknown.

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

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

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

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

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

105 GLUT3 levels were greater in cerebral gray matter than i

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

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

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

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

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

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

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

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

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

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

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

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

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

119 omoted luciferase expression driven by human GLUT3-promoter.

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

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

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

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

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

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

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

127 .5% aa identity with a non-mammalian chicken Glut3 sequence.

128 tituted membrane helix 9 with the equivalent GLUT3 sequence.

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

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

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

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

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

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

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

136 cally active than GLUT3 and GLUT1 containing GLUT3 TM9.

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

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

139 dependent nNOS phosphorylation is coupled to GLUT3 trafficking.

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

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

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

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

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

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

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

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

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

149 GLUT3 was unchanged.

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

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

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

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