ライフサイエンスコーパス: GLAST

1 GLAST and GLT-1 are localized primarily in astrocytes, w

2 GLAST complexes with the extracellular domain of DSCAM.

3 GLAST immunoreactivity indicated no preferential localiz

4 GLAST immunoreactivity was low prenatally but became enr

5 GLAST staining was highest along the stratum pyramidale

6 GLAST was significantly reduced (33.8% +/- 8.1%, mean +/

7 tein of excitatory amino acid transporter 1 (GLAST), which is a major component of astrocytic glutama

8 sporter/excitatory amino acid transporter 1 (GLAST/EAAT1) in EAE cerebellum caused by protein downreg

9 Effects on mRNA expression of glial (GLT-1, GLAST) and neuronal (EAAC1) glutamate transporters in th

10 GLT-1, GLAST, and EAAC1 are high-affinity, Na(+)-dependent glut

11 Long-term lineage tracing in vivo using a GLAST::CreER(T2) conditional driver indicates that alpha

12 In addition, GLAST promoter activation was observed in oligodendrocyt

13 performed with polyclonal antibodies against GLAST and image analysis was carried out with the Image

14 However, in glioma cells, essentially all GLAST protein was found in cell nuclei rather than the p

15 on of glutamate (Glu) transporters GLT-1 and GLAST and attenuated Glu uptake (p < 0.01).

16 ein for the glutamate transporters GLT-1 and GLAST in unique tanycyte populations of the third ventri

17 Reductions in GLT-1 and GLAST may increase the potential for glutamate-induced i

18 ange in cell morphology, increased GLT-1 and GLAST mRNA levels approximately 5-fold, increased GLAST

19 upts glutamate reuptake (decreased GLT-1 and GLAST mRNA).

20 Overall, these studies of GLT-1 and GLAST promoter activity, protein expression, and glutama

21 mical staining indicates that both GLT-1 and GLAST protein are expressed in the tanycyte populations

22 These studies suggest that GLT-1 and GLAST protein are regulated independently in astrocyte c

23 Tsc1 cKO mice exhibit decreased GLT-1 and GLAST protein expression.

24 f the glial glutamate transporters GLT-1 and GLAST was studied in primary cultures derived from corti

25 rn blotting demonstrated that both GLT-1 and GLAST were present at the cell surface.

26 GLT-1 and GLAST were significantly reduced in an experimental rat

27 astrocytic glutamate transporters, GLT-1 and GLAST, and dopaminergic function, including tyrosine hyd

28 astroglial glutamate transporters GLT-1 and GLAST, but not the neuronal transporter EAAC1, restrict

29 astroglial glutamate transporters GLT-1 and GLAST.

30 istry using specific antibodies to GLT-1 and GLAST.

31 d systemic strategy, abolished IL-1beta- and GLAST-dependent synaptopathy in EAE wild-type mice.

32 in the radial glial markers nestin, BLBP and GLAST and later in embryogenesis, the astroglial marker

33 e-dependent downregulation of GTs (EAAC1 and GLAST) in the rat's superficial spinal cord dorsal horn.

34 -III spectrin function by studying EAAT4 and GLAST knockout mice as well as crosses of both with beta

35 usceptible to the combined loss of EAAT4 and GLAST, with degeneration of proximal dendrites, the site

36 C6 glioma expressed EAAC1- but not GLT1- and GLAST-like immunoreactivity.

37 In cortical synaptosomes, EAAC1-, GLT1-, and GLAST-like immunoreactives were apparent.

38 Muller cells Kir2.1, Kir4.1, TASK-1, GS and GLAST expressions and attenuated the peak of inward pota

39 regulated Muller cell Kir4.1, TASK-1, GS and GLAST expressions and enhanced inward potassium currents

40 een identified, named EAAT1-5 in humans, and GLAST, GLT-1, EAAC1, EAAT4, and EAAT5 in rodents, respec

41 rface expression of transferrin receptor and GLAST transporter.

42 ted glutamate accumulation in the retina and GLAST downregulation induced by diabetes mellitus.

43 Increased expression of NFIA, SOX9 and GLAST at the wound site and in the ventricular zone (VZ)

44 including vimentin, nestin, Sox2, Sox9, and GLAST, but not others such as CD15 or GFAP.

45 amino acid transporter EAAT1 (also known as GLAST), but the underlying pathophysiological mechanism

46 NTPDase2 was located to the same membrane as GLAST, indicating that this enzyme is present in type I

47 In primary astrocytes, GLAST protein levels were approximately one half of thos

48 vo, at least in part, by reducing astrocytic GLAST/GLT-1.

49 utamate homeostasis by regulating astrocytic GLAST expression.

50 suggesting a weaker effect at GLT-1 than at GLAST.

51 ped a stellate morphology and expressed both GLAST and GLT-1; neurons expressed only the EAAC1 transp

52 the dBcAMP-treated cultures expressing both GLAST and GLT-1 showed an increase in glutamate uptake V

53 ion of transport in cultures expressing both GLAST and GLT-1, suggesting a weaker effect at GLT-1 tha

54 subtypes have been identified in rat brain; GLAST and GLT-1 are primarily astrocytic, whereas EAAC1

55 A less powerful accumulation of glutamate by GLAST than by GLT-1 cannot be used to explain the high g

56 Glutamate transport by GLAST was found to be driven, as for GLT-1, by the cotra

57 by glutamate through a process triggered by GLAST activity and involving the actin cytoskeleton.

58 caused GLT-1 protein to decrease, and caused GLAST protein to increase.

59 ed cultures of neurons and astrocytes caused GLAST protein to increase approximately 2-fold.

60 otopic in situ hybridization, we demonstrate GLAST mRNA labeling in tanycytes of the ventral floor an

61 wed that cystine did not block Na+-dependent GLAST glutamate transporters (homologous to the transpor

62 ke hypoxia JAK/STAT inhibition downregulates GLAST expression without affecting GLT-1, as demonstrate

63 levels of EAAT2/GLT1, lower levels of EAAT1/GLAST, and the absence of expression of the AMPAR subuni

64 at endfeet and elevated expression of EAAT1/GLAST, with both proteins showing normalized expression

65 All of the cultures expressed GLAST in greater proportion than GLT-1.

66 Finally, GLAST, but not GLT-1, is expressed by specific layers of

67 al GFAP(+) astrocytes, which is critical for GLAST surface distribution and function, and GABAergic t

68 Immunofluorescent labeling for GLAST in IHC supporting cells increased in intensity to

69 Immunogold labeling for GLAST was greater overall in these cells in the 10 mm re

70 Genotype profiles for GLAST; N-methyl-d-aspartate-receptor subunits NR1, NR2A,

71 NFIA is both necessary and sufficient for GLAST induction in the VZ.

72 re of GLAST, and examination of cochlea from GLAST-Discosoma red (DsRed) promoter reporter mice revea

73 of the astrocyte differentiation genes GFAP, GLAST and GS in the absence of extracellular aggrecan.

74 In the pineal gland, GLAST is expressed by astrocytic cells near the pineal s

75 In the pituitary gland, GLAST is likely expressed by folliculo-stellate cells in

76 Recently, four distinct cDNAs (EAAC1, GLT1, GLAST, and EAAT4) encoding Na+-dependent glutamate trans

77 logy and tissue distribution of EAAC1, GLT1, GLAST, and EAAT4, it appears that there are additional g

78 was unique among the subtypes; glycosylated GLAST increased with maturation, whereas nonglycosylated

79 In the adult CNS, the highest GLAST promoter activity was observed in radial glia, suc

80 analyses of cell-surface proteins identified GLAST, a glutamate-aspartate transporter that is marked

81 In GLAST-CreERT2; R26-lsl-GCaMP3 mice, we demonstrate that

82 There was no significant change in GLAST after transection.

83 s of GLT-1 as well as qualitative changes in GLAST (glutamate/aspartate transporter) but no measurabl

84 ficantly modulate gene expression changes in GLAST-1 positive brainstem astrocytes.

85 n also attenuated the Mn-induced decrease in GLAST/GLT-1 mRNA/protein levels in midbrain.

86 There were no significant differences in GLAST or EAAC1 mRNA expression between MCAO and sham-ope

87 glutamate incubation produced an increase in GLAST expression at the astrocyte cell surface.

88 er birth, paralleled by a steady increase in GLAST immunoreactivity and protein content.

89 Neurons induced a small increase in GLAST protein.

90 As was observed with GLT-1, the increases in GLAST protein observed in cocultures were not blocked by

91 transporter 2) and were absent from IPCs in GLAST-/- cochleas.

92 istered at nighttime, a mild hearing loss in GLAST KO mice was found but not at daytime, revealing a

93 oxicity, attenuating Mn-induced reduction in GLAST/GLT-1 expression in murine substantia nigra (SN).

94 inhibition of EAAT1, and its binding site in GLAST has been delineated in an elaborate mutagenesis st

95 mRNA levels approximately 5-fold, increased GLAST protein approximately 2-fold, and increased GLT-1

96 Kir4.1 was down regulated but KCC4, GLAST, microtubule bundles, connexin expression patterns

97 rs, we examined mGluR1 EPSCs in mice lacking GLAST (for glutamate-aspartate transporter; EAAT1) or EA

98 Here, we test in mice lacking GLAST the effects of a low-dose cisplatin known not to c

99 gely by carriers homologous to the mammalian GLAST/EAAT1 transporter.

100 mice, are positive for the astrocyte marker GLAST and the synaptic marker SNAP25, whereas CD11b, a m

101 TREK-1 proteins with the astrocytic markers GLAST and GFAP in rat hippocampal stratum radiatum.

102 nt with detection of the early glial markers GLAST and glutamine synthetase.

103 n in vitro and in vivo A novel mouse mutant (GLAST(CreERT2)::Cox10(flox/flox)) was generated, in whic

104 ults uncover an unrecognized pathway of NEO1-GLAST in hippocampal GFAP(+) astrocytes, which is critic

105 kainate, plus a trace amount of GLT1, but no GLAST.

106 tential therapeutic target to restore normal GLAST expression and uptake of glutamate after perinatal

107 hese results indicate that (i) EAAC1 but not GLAST or GLT1 transporters are expressed in C6 glioma, (

108 ut GLAST or blocking GLT-1 in the absence of GLAST greatly prolonged and enhanced the AMPA receptor-m

109 t GLAST, or blocking GLT-1 in the absence of GLAST, prolonged the EPSC when many parallel fibres were

110 Riluzole, as an activator of GLAST-mediated uptake, rescues the proximal impairment i

111 nteracting protein decreases the affinity of GLAST transporters.

112 termini, increases the glutamate affinity of GLAST.

113 lutamate clearance and the delocalization of GLAST away from the cleft of parallel fibre (PF) synapse

114 This study compares the distribution of GLAST and GLT-1 expression in the circumventricular orga

115 l disorders associated with dysregulation of GLAST/GLT-1.

116 The continued expression of GLAST by these neural progenitors raises the possibility

117 ults suggest that cell-surface expression of GLAST can be rapidly regulated by glutamate through a pr

118 and examined the differential expression of GLAST in the spiral ligament of the basal, middle, and a

119 nvolved in modulating regional expression of GLAST.

120 ression of GLT-1 and increased expression of GLAST.

121 cited by L-glutamate, a prominent feature of GLAST, and examination of cochlea from GLAST-Discosoma r

122 rs regulating the expression and function of GLAST and GLT-1 in their native cell type.

123 opurine attenuated the increased function of GLAST-overexpressing HSCs.

124 is a remarkable subcellular heterogeneity of GLAST and GLT-1 expression in the developing hippocampus

125 one (VZ) concomitantly with the induction of GLAST, an early marker of gliogenesis.

126 Until now, the involvement of GLAST in cisplatin-mediated ototoxicity remains unknown.

127 ures had 2- to 4-times increase in levels of GLAST and GLT-1-mRNA expression both before and after sc

128 Yet the loss of GLAST appears to be independent of EAAT4 loss, highlight

129 per-excitability and that subsequent loss of GLAST, superimposed on the earlier deficiency of EAAT4,

130 dysfunction underpin the pathogenic loss of GLAST.

131 ay reduction of GLT-1 and mislocalization of GLAST.

132 The post-translational modification of GLAST was unique among the subtypes; glycosylated GLAST

133 aminar and subcellular expression profile of GLAST and GLT-1 in the developing postnatal mouse hippoc

134 d (l-trans-PDC) or by partial suppression of GLAST using siRNA interference.

135 We show that the auditory synapse of GLAST KO mice is more vulnerable to cisplatin administra

136 a changed with a gradient similar to that of GLAST labeling.

137 ity of EAAC1 and GLT-1 compared with that of GLAST.

138 f several residues in TM3, TM4c, and TM7a of GLAST have detrimental effects on the inhibitory potency

139 are absent from the choroid plexus, and only GLAST mRNA is found in the subcommisural organ.

140 Compared with astrocytes expressing only GLAST, the dBcAMP-treated cultures expressing both GLAST

141 [(3)H]l-glutamate uptake in OLs than GLT1 or GLAST.

142 Expressing NEO1 or GLAST in Neo1 KO astrocytes in the hippocampus abolishes

143 ially directed glial processes (vimentin- or GLAST-immunolabeled fibers) spanning through the CC.

144 er subtype 1 (EAAT1) and its rodent ortholog GLAST are elucidated.

145 mall number of parallel fibres, knocking out GLAST or blocking GLT-1 in the absence of GLAST greatly

146 Knocking out GLAST, or blocking GLT-1 in the absence of GLAST, prolon

147 targeted expression to the nestin(+)/Pax6(+)/GLAST(+) radial glial cells and Tbr2(+) intermediate pro

148 he lamina terminalis, and the area postrema, GLAST is strongly expressed, whereas GLT-1 is faintly ex

149 NEO1 interacts with GLAST and promotes GLAST surface distribution in astrocytes.

150 replicated EAE modifications through a rapid GLAST/EAAT1 downregulation, whereas incubation of an IL-

151 mice cerebral cortex also displayed reduced GLAST and GLT-1 expression.

152 n vitro studies have shown that Mn repressed GLAST and GLT-1 via activation of transcription factor Y

153 t to other studies with non-human specimens, GLAST was expressed in the spiral ligament fibrocytes bu

154 The strong GLAST expression by the ventral tanycytes in the hypophy

155 glial-specific glutamate transporter subtype GLAST.

156 and immunohistochemistry to assess YY1, TH, GLAST, and GLT-1 levels.

157 These data indicate that GLAST in supporting cells is responsible for transmitter

158 ural progenitors raises the possibility that GLAST may have an unanticipated role in regulating their

159 These results show that GLAST is the primary glutamate transporter in the circum

160 Our data also showed that GLAST expression significantly differs in the basal and

161 The GLAST promoter is active in both radial glia and many as

162 y murine astrocyte cultures that express the GLAST (EAAT1) and GLT-1 (EAAT2) transporter subtypes.

163 post-hoc analysis showed a difference in the GLAST immunoreactive area of patients with Meniere's dis

164 nslocation through the other monomers in the GLAST trimer.

165 rotein and the last eight amino acids of the GLAST C-terminus, which have some similarity to the PDZ

166 interactions of the C- and N-termini of the GLAST glutamate transporter with other proteins, we dial

167 crevice in the "trimerization domain" of the GLAST monomer, and the inhibitor is demonstrated to inhi

168 ed astrocyte monocultures expressed only the GLAST subtype.

169 Removing the GLAST C-terminus interaction increases the transporter c

170 This GLAST mRNA labeling had a higher intensity than the labe

171 Thus, GLAST and GLT-1 curtail the EPSC produced by a single st

172 ve been cloned from animal and human tissue: GLAST (EAAT1), GLT-1 (EAAT2), EAAC1 (EAAT3), EAAT4, and

173 oduction (glutaminase), glutamate transport (GLAST, GLT-1 and EAAT-1), glutamate metabolism (glutamat

174 ransporters (glutamate/aspartate transporter GLAST, Na(+)/Cl(-) transporter NTT4/Rxt1), enzymes (aryl

175 ions in the astrocytic glutamate transporter GLAST expressed in Bergmann glia.

176 Bergmann glia-specific glutamate transporter GLAST was reduced in Gfa2-SCA7 mice and was associated w

177 predominant cerebellar glutamate transporter GLAST, expressed in Bergmann glia, only fall progressive

178 affect the astrocytic glutamate transporter GLAST, nor did it block glutamate release via the P2X(7)

179 c stoichiometry of the glutamate transporter GLAST, which is the major glutamate transporter expresse

180 ions of the glutamate-aspartate transporter (GLAST or excitatory amino acid transporter 1), vesicular

181 ransporters glutamate-aspartate transporter (GLAST) and glutamate transporter 1 (GLT-1) are reduced.

182 Glutamate/aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) are the most

183 ansporters, glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1), which are es

184 GS) and L-Glutamate/L-Aspartate Transporter (GLAST) functions.

185 The glutamate-aspartate transporter (GLAST) has been shown to exist and function within non-h

186 so known as glutamate aspartate transporter (GLAST) in rodents, is one of two glial glutamate transpo

187 The glutamate aspartate transporter (GLAST) shields the auditory synapse from excessive gluta

188 transporter glutamate/aspartate transporter (GLAST) were also determined.

189 y targeting glutamate-aspartate transporter (GLAST), a crucial glial transporter involved in glutamat

190 t the glial glutamate/aspartate transporter (GLAST), the transduction pathway proteins phospholipase

191 f the glial glutamate-aspartate transporter (GLAST), which causes an enhancement of the glutamatergic

192 y targeting glutamate aspartate transporter (GLAST)-expressing cells, replicates such alterations.

193 LDH1L1) and Glutamate Aspartate Transporter (GLAST); the reactive markers: Glial Fibrillary Acidic Pr

194 cosoma red [glutamate-aspartate transporter (GLAST)] and green fluorescent protein [glutamate transpo

195 vels of another glial glutamate transporter, GLAST.

196 drial markers and the glutamate transporter, GLAST.

197 ed in rat, including astroglial transporters GLAST and GLT-1 and a neuronal transporter EAAC1.

198 The glial glutamate transporters GLAST and GLT-1 are primarily responsible for the remova

199 e show that the glial glutamate transporters GLAST and GLT-1 limit the activation of Purkinje cell AM

200 The loss of glial glutamate transporters GLAST or GLT-1 produced elevated extracellular glutamate

201 ice lacking the glial glutamate transporters GLAST or GLT-1, the ischaemia-evoked AD current was indi

202 roduced by glutamate-aspartate transporters (GLAST) (excitatory amino acid transporter 1) because the

203 ltures expressed the two glial transporters, GLAST and GLT-1, while none of the cultures expressed th

204 Two glutamate transporters, GLAST (EAAT-1) and GLT-1 (EAAT-2), were studied by immun

205 of the electrogenic glutamate transporters, GLAST, GLT-1, and EAAC-1, was quantitated by the reverse

206 Two of the three transporters, GLAST (EAAT1) and EAAC1 (EAAT3), are localized to microc

207 rgic and GABAergic transmissions, along with GLAST/EAAT1 normalization, milder inflammation, and redu

208 NEO1 interacts with GLAST and promotes GLAST surface distribution in astrocy

209 nexpectedly in a nonoverlapping pattern with GLAST.