ライフサイエンスコーパス: EAAT2

1 of the excitatory amino acid transporter 2 (EAAT2) .

2 of the excitatory amino acid transporter 2 (EAAT2).

3 , the ortholog of mammalian astrocytic GLT1 (EAAT2).

4 tatory amino-acid transporter 1 (EAAT1), and EAAT2.

5 uptake and heteroexchange are comparable in EAAT2.

6 nion current amplitudes for L46P than for WT EAAT2.

7 and attenuated the Mn-induced repression of EAAT2.

8 mate, via neurotransmitter transport by GLT1/EAAT2.

9 s in the necrotic foci in PVL also expressed EAAT2.

10 astrocytic glutamate transporters EAAT1 and EAAT2.

11 predominant forebrain glutamate transporter, EAAT2.

12 gate IKKbeta- and p65-mediated activation of EAAT2.

13 its both basal and p65-induced activation of EAAT2.

14 ding to a 59- and 45-fold selectivity toward EAAT2.

15 port is handled by the glutamate transporter EAAT2.

16 e through reducing the glutamate transporter EAAT2.

17 HNE was the astrocytic glutamate transporter EAAT2.

18 n, we synthesized novel activators (4a-f) of EAAT2.

19 in the promoter of rat Slc1a2 gene encoding EAAT2.

20 GLT-1 and excitatory amino acid transporter EAAT2.

21 her suggest the presence of a sodium leak in EAAT2.

22 tumor necrosis factor alpha (TNF-alpha), on EAAT2.

23 NA levels of the glial glutamate transporter EAAT2, a protein regulated by GRM3 that critically modul

24 te-mediated excitotoxic injury and death via EAAT2 activation.

25 LDN-212320 (3) was found to be a potent EAAT2 activator at a translational level, restoring the

26 prolongs survival, and ceftriaxone increases EAAT2 activity.

27 ggest EAAT2b transports glutamate similar to EAAT2, although the contribution of EAAT2b to normal cle

28 mains revealed that a large portion of total EAAT2 and a minor portion of total EAAT1, EAAT3, and EAA

29 EAAT2 and AQP4 colocalization was also reduced in the st

30 Our data suggest that EAAT2 and AQP4 exist in astrocytic membranes as a macrom

31 gesting that ENT1-mediated downregulation of EAAT2 and AQP4 expression contributes to excessive ethan

32 indicate that adenosine signaling regulates EAAT2 and astrocytic AQP4 expressions, which control eth

33 se to two fragments that we termed truncated EAAT2 and COOH terminus of EAAT2 (CTE).

34 inhibitor at EAAT1 (IC50 20 muM) compared to EAAT2 and EAAT3 (IC50 > 300 muM).

35 city of UCPH-101 and UCPH-102 for EAAT1 over EAAT2 and EAAT3 is demonstrated to extend to the EAAT4 a

36 EAAT1 with a 14- and 9-fold preference over EAAT2 and EAAT3, respectively.

37 exploration of the therapeutic potential of EAAT2 and may provide molecular insights into mechanisms

38 itical negative transcriptional regulator of EAAT2 and mediates Mn-induced EAAT2 repression.

39 r Yin Yang 1 (YY1) is critical in repressing EAAT2 and mediates the effects of negative regulators, s

40 st that NF-kappaB can intrinsically activate EAAT2 and that TNFalpha mediates repression through a di

41 e to generate transgenic mice overexpressing EAAT2 and then to cross these mice with the ALS-associat

42 related to ALS, including downregulation of Eaat2 and upregulation of Tnfrsf1a.

43 plasmalemmal glial-glutamate transporter 2 (EAAT2) and increased vesicular glutamate transporter-1 (

44 for glutamate exist on astrocytes (EAAT1 and EAAT2) and neurons (EAAT3).

45 xpression of the glutamate transporter Glt1 (EAAT2) and protects these animals from death.

46 of type 2 excitatory amino-acid transporter (EAAT2) and the astrocyte-specific water channel, aquapor

47 romoter of astroglial glutamate transporter (EAAT2) and the same approach was initially used here to

48 ased glutamate uptake, a primary function of EAAT2, and EAAT2 small interference RNA completely inhib

49 cDNA for EAAT1, EAAT2, and EAAT3 was observed, indicating that mRNA was

50 ry amino acid transporter transcripts EAAT1, EAAT2, and EAAT3 was performed in discrete thalamic nucl

51 s found to be approximately 1:3:6 for EAAT1, EAAT2, and EAAT3, respectively.

52 nst the full-length coding regions of EAAT1, EAAT2, and EAAT3.

53 atory amino acid transporter subtypes EAAT1, EAAT2, and EAAT3.

54 selectivity made gluconate permeant in L46P EAAT2, and nonstationary noise analysis revealed slightl

55 r subunits, glutamate transporters EAAT1 and EAAT2, and the GABA(A) receptor.

56 er (DAT) and the glial glutamate transporter EAAT2, and we identified a conserved serine residue in F

57 L46 is a pore-forming residue of the EAAT2 anion channels at the cytoplasmic entrance into th

58 s to quantify absolute open probabilities of EAAT2 anion channels from ratios of anion currents by gl

59 increased absolute open probability of L46P EAAT2 anion channels.

60 creased unitary current amplitudes in mutant EAAT2 anion channels.

61 an important determinant of the diameter of EAAT2 anion pore and demonstrate the existence of anion

62 and impairment in expression and activity of EAAT2 are two distinct molecular mechanisms occurring in

63 that the glutamate transporters, especially EAAT2, are associated with cholesterol-rich lipid raft m

64 it EAAT2 by triggering caspase-3 cleavage of EAAT2 at a single defined locus.

65 rt the novel evidence that caspase-3 cleaves EAAT2 at a unique site located in the cytosolic C-termin

66 EAAT2 block also augmented action potential discharge in

67 Astrocytic EAAT2 buffers basal glutamate activation of AMPA-type gl

68 2 expression and function, elevated not only EAAT2 but also AQP4 expression in the striatum.

69 xpressions of transcripts encoding EAAT1 and EAAT2, but not EAAT3, were detected in the thalamus of s

70 proteins exposed to oxidative stress inhibit EAAT2 by triggering caspase-3 cleavage of EAAT2 at a sin

71 Using EAAT2 constructs with an extracellular biotin acceptor t

72 ism by which the glial glutamate transporter EAAT2 could contribute to the pathology of ALS.

73 The loss of functional EAAT2 could lead to the accumulation of extracellular gl

74 termed truncated EAAT2 and COOH terminus of EAAT2 (CTE).

75 Astrocytic EAAT2 deficiency also shows transcriptomic overlaps with

76 on of the kynurenine pathway, and astrocytic EAAT2 deficiency results in dysfunction of innate and ad

77 iles associated with astrocytic and neuronal EAAT2 deletion are substantially different, with the for

78 Neuronal EAAT2 deletion leads to dysregulation of the kynurenine

79 Astrocytic, but not neuronal EAAT2, deletion leads to early deficits in short-term me

80 mechanisms: complement activation, AQP4 and EAAT2 down-regulation, and disruption of glutamate homeo

81 Since glutamate toxicity caused by EAAT2 dysfunction is thought to promote several differen

82 imal and human tissue: GLAST (EAAT1), GLT-1 (EAAT2), EAAC1 (EAAT3), EAAT4, and EAAT5.

83 d analogous effects on GltPh simulations and EAAT2/EAAT4 measurements of single-channel currents and

84 and the peak amplitude of iGlu (u) Finally, EAAT2 (excitatory amino acid transport protein 2) immuno

85 edominant astroglial L-glutamate transporter EAAT2 (excitatory amino acid transporter 2) does not con

86 EAAT2 (excitatory amino acid transporter 2) is a high af

87 loss of the astroglial glutamate transporter EAAT2 (excitatory amino acid transporter 2) protein in m

88 ne, an antibiotic compound known to increase EAAT2 expression and function, elevated not only EAAT2 b

89 ain constant, indicating that alterations in EAAT2 expression are due to disturbances at the post-tra

90 ndicate that strategies designed to increase EAAT2 expression have potential for preventing excitotox

91 Despite the lower level of EAAT2 expression in glutamatergic terminals, when hippoc

92 mmunohistochemistry confirmed an increase in EAAT2 expression in hippocampus, identifying a possible

93 the mechanism by which ceftriaxone enhances EAAT2 expression in primary human fetal astrocytes (PHFA

94 ility and experience-dependent regulation of EAAT2 expression in the dorsal striatum, mice were train

95 This work demonstrates that plasticity of EAAT2 expression in the lateral part of the dorsal stria

96 cell- and region-level studies of EAAT1 and EAAT2 expression in the mediodorsal nucleus of the thala

97 The regulation of EAAT2 expression involves actin polymerization-dependent

98 Previously, we found that EAAT2 expression is limited primarily to premyelinating

99 EAAT2 expression is reduced in aging and sporadic Alzhei

100 Increased EAAT2 expression protects neurons from L-glutamate induc

101 glutamate transport in BTSCs with high EAAT1/EAAT2 expression rendered cells susceptible to GLS inhib

102 ed repression and EGF-mediated activation of EAAT2 expression require NF-kappaB.

103 veral classes of compounds that can increase EAAT2 expression through translational activation.

104 We manipulated EAAT2 expression using chemogenetic activation of astroc

105 beta-lactam antibiotics, is a stimulator of EAAT2 expression with neuroprotective effects in both in

106 rocytes decreased TNFR1 levels and increased EAAT2 expression, and improved motor neuron survival.

107 that transcriptional processes can regulate EAAT2 expression.

108 remature death, confirming the importance of EAAT2 for brain function and validating the genetic cons

109 ibition of GLT-1 [for glutamate transporter; EAAT2 (for excitatory amino acid transporter)] with dihy

110 tin-cyclization recombinase (Cre) eliminated EAAT2 from the brain, resulting in epilepsy and prematur

111 Reduced EAAT2 function could lead to accumulation of extracellul

112 interest to discover selective modulators of EAAT2 function.

113 otential tool for the further elucidation of EAAT2 function.

114 sporter studies demonstrated a large loss of EAAT2 function.

115 of astrocytic glutamate transporter (GLT-1; EAAT2) function is associated with multiple neurodegener

116 Furthermore, our EAAT2/G93A double transgenic mice showed a statistically

117 haracterized the genomic organization of the EAAT2 gene and used single-strand conformation polymorph

118 dies indicate that germline mutations in the EAAT2 gene are infrequent and do not explain the presenc

119 Here we floxed the EAAT2 gene to produce the first conditional EAAT2 knock-

120 sis revealed reduced transcripts of Gad1 and Eaat2 genes, which code for enzymes involved in the synt

121 f the high-affinity glutamate transporter 1 (EAAT2/GLT-1) in the nucleus accumbens (NAc).

122 The glutamate transporter gene, EAAT2/GLT-1, is induced by epidermal growth factor (EGF)

123 Focal loss of the EAAT2 glutamate transporter in the ventral horn of the s

124 The EAAT2 glutamate transporter, accounts for >90% of hippoc

125 ion, by studying the expression of EAAT1 and EAAT2 glutamate transporters, it was possible to documen

126 lutamate from the synaptic cleft and loss of EAAT2 has been previously reported in amyotrophic latera

127 pts for the astroglial glutamate transporter EAAT2 have been detected in brain tissues of 60% of pati

128 s the most potent and selective inhibitor of EAAT2 identified to date.

129 showed a significantly higher percentage of EAAT2-immunopositive astrocytes in PVL (51.8% +/- 5.6%)

130 in vivo resulted in the formation of larger EAAT2-immunoreactive clusters on the cell surface.

131 , which appeared concurrently to the loss of EAAT2 immunoreactivity and to increased expression of ac

132 and glutamate that resembles original GLT-1/EAAT2 in all tested functional aspects.

133 These findings suggest that the loss of EAAT2 in ALS is due to aberrant mRNA and that these aber

134 Marked reduction of EAAT2 in AQP4-deficient regions of NMO patient spinal co

135 In this study, we analyzed the expression of EAAT2 in cerebral white matter from PVL and control case

136 t mediate TX-induced up-regulation of GLT-1 (EAAT2 in humans), we investigated its effect on GLT-1 at

137 king finding was the transient expression of EAAT2 in layer V pyramidal neuronal cell bodies up until

138 the presence of variant mRNA transcripts of EAAT2 in more than one-half of ALS cases.

139 Double-label immunocytochemistry detected EAAT2 in OLs but not astrocytes or axons in the human fe

140 blot analysis suggested an up-regulation of EAAT2 in PVL compared with control cases.

141 The expression of EAAT2 in pyramidal neurons during human brain developmen

142 The previously unrecognized up-regulation of EAAT2 in reactive astrocytes and its presence in macroph

143 ethanol withdrawal-induced downregulation of EAAT2 in the striatum.

144 sporter excitatory amino acid transporter 2 (EAAT2) in LPS-treated astrocytes.

145 ter was responsible for ceftriaxone-mediated EAAT2 induction.

146 lled by the astrocytic glutamate transporter EAAT2, influencing synaptic functioning and neural netwo

147 tion and cardiorespiratory effects following EAAT2 inhibition were due to activation of putative extr

148 F3-phenyl analogue 4r was a potent selective EAAT2-inhibitor (IC50 = 2.8 muM) exhibiting 30- and 50-f

149 his site and identified a selective class of EAAT2 inhibitors that were tested in glutamate uptake an

150 d computational methods to identify specific EAAT2 inhibitors.

151 aluating both the stimulation of currents in EAAT2-injected oocytes and the heteroexchange of d-[(3)H

152 EAAT2 is a high affinity, Na+-dependent glutamate transp

153 ompound treatment cessation, suggesting that EAAT2 is a potential disease modifier with therapeutic p

154 Glial recordings confirmed EAAT2 is functional on nTS astrocytes.

155 Dysfunction of EAAT2 is implicated in acute and chronic neurological di

156 emonstrate that normal function of EAAT1 and EAAT2 is necessary for retinal ganglion cell survival an

157 astrocyte endocytosis of NMO-IgG, AQP4, and EAAT2 is not a significant consequence of AQP4 autoantib

158 findings suggest that caspase-3 cleavage of EAAT2 is one mechanism responsible for the impairment of

159 Although EAAT2 is predominantly expressed in astrocytes, approxim

160 The glial glutamate transporter EAAT2 is primarily responsible for clearance of glutamat

161 l of the disease, expression and activity of EAAT2 is remarkably reduced.

162 ies demonstrate that under normal conditions EAAT2 is specific to astrocytes.

163 The glial glutamate transporter EAAT2 is the main mediator of glutamate clearance.

164 Since EAAT2 is the most expressed EAAT in the nTS, this study

165 Excitotoxicity caused by down-regulation of EAAT2 is thought to be a contributing factor to motor ne

166 Excitatory amino acid transporter-2 (EAAT2) is a major glutamate transporter in the brain exp

167 POINTS: Excitatory amino acid transporter 2 (EAAT2) is present on astrocytes in the nucleus tractus s

168 The excitatory amino acid transporter 2 (EAAT2) is the major glutamate transporter in the brain e

169 t was observed using inhibitors specific for EAAT2 (kainic acid and dihydrokainic acid) and EAAT3 (cy

170 EAAT2 gene to produce the first conditional EAAT2 knock-out mice.

171 A truncated splice variant of EAAT2, known as EAAT2b, also has been identified in astr

172 QP4 and the associated glutamate transporter EAAT2, leading to glutamate excitotoxicity.

173 Caspase-3 cleavage of EAAT2 leads to a drastic and selective inhibition of thi

174 Loss of EAAT2 leads to increased extracellular glutamate and exc

175 Further, reduced membralin and EAAT2 levels correlated with disease progression in spin

176 Restoring EAAT2 levels in membralin KO astrocytes limited astrocyt

177 phic lateral sclerosis motor cortex, whereas EAAT2 levels were decreased by up to 95%.

178 tochemistry, and proteome analysis) that the EAAT2 levels were too low to support any of the four hyp

179 mutant SOD1 ALS mice of a truncated form of EAAT2, likely deriving from caspase-3-mediated proteolyt

180 At end-stage disease, gliosis increased and EAAT2 loss in the ventral horn exceeded 90%, suggesting

181 Neuronal EAAT2 loss results in late-onset spatial reference long-

182 have tested the hypothesis that the gene for EAAT2 may be defective in some ALS cases.

183 These results suggest that the loss of EAAT2 may contribute to, but does not cause, motor neuro

184 een the distribution of EAAT2 protein and of EAAT2-mediated transport activity.

185 Glial glutamate transporter EAAT2-mediated uptake was more sensitive to this effect.

186 GLT-1 (EAAT2) mediates the bulk of this activity in forebrain.

187 EAAT2 modulates cardiorespiratory control and tempers ex

188 xpressed in astrocytes, approximately 10% of EAAT2 molecules are found in axon terminals.

189 EAAT2 mRNA levels, however, remain constant, indicating

190 Multiple EAAT2 mRNA transcripts have been described, but those re

191 EAAT2 mRNA was abundant in human fetal white matter duri

192 Multiple abnormal EAAT2 mRNAs, including intron-retention and exon-skippin

193 addition to the widely recognized astrocytic EAAT2, neuronal EAAT2 plays a role in hippocampus-depend

194 mportantly, this translational regulation of EAAT2 occurred in vivo (i.e. both in primary cortical ne

195 We conclude that transient expression of EAAT2 occurs during the window of peak vulnerability for

196 novo variants were found only in SLC1A2 (aka EAAT2 or GLT1) (c.244G>A [p.Gly82Arg]) and YWHAG (aka 14

197 were not significantly different for EAAT1, EAAT2, or EAAT3, but 2-FAA exhibited higher affinity for

198 pressing the human transporter clones EAAT1, EAAT2, or EAAT3, it was found that the pharmacological p

199 ecreased excitatory aminoacid transporter 2 (EAAT2) overexpression delays disease onset and prolongs

200 Glial glutamate transporter EAAT2 plays a major role in glutamate clearance in synap

201 The astroglial glutamate transporter EAAT2 plays a major role in maintaining low levels of ex

202 widely recognized astrocytic EAAT2, neuronal EAAT2 plays a role in hippocampus-dependent memory.

203 s indicated that glial glutamate transporter EAAT2 plays an essential role in cognitive functions and

204 The role EAAT2 plays in cognitive aging and its associated mechan

205 d new light on the important role astrocytic EAAT2 plays on buffering nTS excitation and overall card

206 transport in PHFA through NF-kappaB-mediated EAAT2 promoter activation.

207 Mn decreases EAAT2 promoter activity and mRNA and protein levels, but

208 and, accordingly, HDAC inhibitors increased EAAT2 promoter activity and reversed the Mn-induced repr

209 YY1 overexpression in astrocytes reduced EAAT2 promoter activity, while YY1 knockdown or mutation

210 ty and reversed the Mn-induced repression of EAAT2 promoter activity.

211 or mutation of the YY1 consensus site of the EAAT2 promoter increased its promoter activity and atten

212 ey raise the intriguing possibility that the EAAT2 promoter may be useful for targeting gene expressi

213 This led to increased YY1 binding to the EAAT2 promoter region.

214 ing only one of the co-inherited SNPs in the EAAT2 promoter to human diseases.

215 g.-168C > T giving a rise to a total of ten EAAT2 promoter variants.

216 paB binding site at the -272 position of the EAAT2 promoter was responsible for ceftriaxone-mediated

217 ntly, we find that N-myc is recruited to the EAAT2 promoter with TNFalpha and that N-myc-binding site

218 he cloning and characterization of the human EAAT2 promoter, demonstrating elevated expression in ast

219 leoprotein K (hnRNP K), which binds the GLT1/EAAT2 promoter.

220 rent study, we investigated whether restored EAAT2 protein and function could benefit cognitive funct

221 plained mismatch between the distribution of EAAT2 protein and of EAAT2-mediated transport activity.

222 We show that the amount of EAAT2 protein and the associated Na+-dependent glutamate

223 y play an important role in the differential EAAT2 protein expression under normal and disease condit

224 m both approaches demonstrated that restored EAAT2 protein function significantly improved cognitive

225 role in cognitive functions and that loss of EAAT2 protein is a common phenomenon observed in AD pati

226 These results indicate that expression of EAAT2 protein is highly regulated at the translational l

227 Transport-competent EAAT2 protein is up-regulated in differentiating astrocy

228 hic lateral sclerosis and Alzheimer disease, EAAT2 protein levels are significantly decreased in affe

229 Immunoblotting demonstrated that EAAT2 protein was highly expressed in early development

230 The transgenic EAAT2 protein was properly localized to the cell surface

231 tion in excitatory amino acid transporter 2 (EAAT2) protein levels in astrocyte cultures, which was b

232 wever, RFX1 did not change the expression of EAAT2 proteins in the NRK52E cells.

233 and activity of glutamate uptake transporter EAAT2, reduces the occurrence or severity of ethanol wit

234 he glutamate transporter GLT1 (also known as EAAT2; refs 1, 2), the physiologically dominant astrogli

235 Since the pharmacologic activation of EAAT2 represents a valuable strategy to relieve neuropat

236 s, but the molecular mechanism of Mn-induced EAAT2 repression at the transcriptional level has yet to

237 l regulator of EAAT2 and mediates Mn-induced EAAT2 repression.

238 However, it remains unclear if EAAT2 responds to environmental cues to specifically sha

239 produce a dominant negative effect on normal EAAT2 resulting in loss of protein and activity.

240 ditional deletion of astrocytic and neuronal EAAT2 results in age-related cognitive deficits.

241 ecially excitatory amino acid transporter 2 (EAAT2, rodent analog GLT1) to regulate extracellular glu

242 known to increase the glutamate transporter EAAT2's ability to scavenge excess glutamate, regulating

243 the nTS, this study specifically determined EAAT2's role in nTS astrocytes, its influence on neurona

244 amate (excitatory amino acid) transporter 2 (EAAT2; Slc1a2) has been hypothesized to (a) provide isle

245 GLT-1 (EAAT2; slc1a2) is the major glutamate transporter in the

246 ate uptake, a primary function of EAAT2, and EAAT2 small interference RNA completely inhibited ceftri

247 ion of glutamate transporters with either an EAAT2 specific inhibitor or a nonspecific inhibitor of a

248 The EAAT2-specific antagonist dihydrokainate (DHK) was micro

249 sitive to dihydrokainic acid (DHKA), a known EAAT2-specific inhibitor.

250 ized two retinal EAATs from mouse, the GLT-1/EAAT2 splice variant GLT-1c, and EAAT5.

251 ed with low concentration of d-aspartate (an EAAT2 substrate), axon terminals accumulate d-aspartate

252 m exhibited the greatest similarity with the EAAT2 subtype, a transporter believed to be expressed pr

253 rtate (TBOA) but was insensitive to the GLT1/EAAT2 subtype-selective antagonist dihydrokainate and wa

254 The kinetic properties of EAAT2, the dominant glutamate transporter in brain astro

255 The gene for EAAT2, the major astrocytic glutamate transporter, gener

256 howed no significant change in the amount of EAAT2, the predominant glial glutamate transporter in th

257 opionic acid analogs as potent inhibitors of EAAT2, the predominant glutamate transporter in forebrai

258 familial form of ALS leads to inhibition of EAAT2 through a mechanism that largely involves activati

259 ateral-preferring EAAT1 and the nonpolarized EAAT2 to the apical surface.

260 rol significantly altered the trafficking of EAAT2 to the plasma membrane as well as their membrane d

261 sistent with the predominant contribution of EAAT2 to this activity.

262 astrocyte line that constantly expressed an EAAT2 transcript containing the 565-nt 5'-UTR and found

263 nsitive and reliable quantitative measure of EAAT2 transcript copy ratios.

264 Ceftriaxone elevated EAAT2 transcription in PHFA through the nuclear factor-k

265 r (TNFR1)-NFkappaB pathway known to suppress Eaat2 transcription was upregulated with membralin delet

266 transport, both positive and negative, alter EAAT2 transcription, promoter activity, mRNA, and protei

267 Neuron-stimulated KBBP is required for GLT1/EAAT2 transcriptional activation and is responsible for

268 In the present study, we found that some EAAT2 transcripts contained 5'-untranslated regions (5'-

269 LS is not associated with elevated levels of EAAT2 transcripts retaining intron 7 and skipping exon 9

270 A transgenic mouse approach via crossing EAAT2 transgenic mice with APPSw,Ind.

271 ate uptake was increased about 2-fold in our EAAT2 transgenic mice.

272 e that the use of small molecules to enhance EAAT2 translation may be a therapeutic strategy for the

273 al. characterize a compound that upregulates EAAT2 translation, thereby increasing glutamate uptake b

274 1) activation, which regulates activation of EAAT2 translation.

275 and a pharmacological approach using a novel EAAT2 translational activator, LDN/OSU-0212320, were con

276 t Parawixin1 does not stimulate uptake by an EAAT2 transport mutant (E405D) defective in the potassiu

277 Regulators of EAAT2 transport, both positive and negative, alter EAAT2

278 e report that the L46P mutation in the human EAAT2 transporter fulfills this prediction.

279 ctive enhancement of glutamate influx by the EAAT2 transporter subtype through a mechanism that does

280 es that express the GLAST (EAAT1) and GLT-1 (EAAT2) transporter subtypes.

281 aster than previously reported for expressed EAAT2 transporters or the efficiency of these transporte

282 regions of the genes encoding for EAAT1 and EAAT2, two glial EAATs.

283 licing of the dominant glutamate transporter EAAT2 under conditions of neurological stress.

284 Interfering with EAAT2 upregulation in this striatal area preserves behav

285 regulate astroglial synaptic functions, GLT1/EAAT2, via kappa B-motif binding phosphoprotein (KBBP),

286 EAAT2 was also expressed in neurons in layer I (presumed

287 The specific role of nTS EAAT2 was determined via whole animal and brainstem slic

288 With western blotting, we found that EAAT2 was expressed as a single band until 2 postnatal m

289 e or no internalization of NMO-IgG, AQP4, or EAAT2 was found in primary astrocyte cultures, nor was g

290 tency determined for the inhibition of human EAAT2 was N(4)-[4-(2-bromo-4,5-difluorophenoxy)phenyl]-L

291 Utilizing a homology model of human EAAT2, we identified a binding pocket at the interface o

292 in our previous model of glutamate uptake by EAAT2, we predict that the voltage sensitivity of exchan

293 nt mouse models, and reductions in membralin/EAAT2 were observed in human ALS spinal cord.

294 ies of the excitatory amino acid transporter EAAT2 were studied using rapid applications of L-glutama

295 ion of the human glutamate transporter GLT1 (EAAT2), which had been detected in a patient with sporad

296 The glutamate transporter EAAT2, which is primarily localized on astrocytic proces

297 ining is associated with the upregulation of EAAT2, which results in enhanced glutamate clearance and

298 ex was largely confined to the neuropil-like EAAT2, with occasional faint neuronal expression.

299 ytes in both PVL and control cases expressed EAAT2, without qualitative difference in expression.

300 igate whether supplementation of the loss of EAAT2 would delay or rescue the disease progression.