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1 GLT-1 (EAAT2) mediates the bulk of this activity in fore
2 GLT-1 (EAAT2; slc1a2) is the major glutamate transporter
3 GLT-1 and GLAST were significantly reduced in an experim
4 GLT-1 exhibited a laminar expression pattern from P10-15
5 GLT-1 is responsible for the majority of glutamate uptak
6 GLT-1 promoter activity in the adult CNS is almost compl
7 GLT-1, GLAST, and EAAC1 are high-affinity, Na(+)-depende
8 GLT-1, the major glutamate transporter in the adult brai
9 GLT-1-like immunoreactivity localized to the inner capsu
10 the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens cor
11 been attributed to glutamate transporter 1 (GLT-1) and xCT (a catalytic subunit of Sxc)/Sxc upregula
13 ion and function of glutamate transporter 1 (GLT-1) in rat astrocytes, an effect that was mediated by
14 d increase in glial glutamate transporter 1 (GLT-1) mRNA expression and the phosphorylation of cAMP-r
15 lation of the glial glutamate transporter 1 (GLT-1) on astrocytes and to reduce peri-ischemic extrace
16 duced expression of glutamate transporter-1 (GLT-1) and occurs concurrent with tau inclusion patholog
17 sporter (GLAST) and glutamate transporter-1 (GLT-1) are the most abundant subtypes and are essential
20 sporter (GLAST) and glutamate transporter-1 (GLT-1), which are essential for the maintenance of low e
21 cytic expression of glutamate transporter-1 (GLT-1), which would prevent excitotoxic-induced neuronal
25 tified that after mutation to alanine (6L/6A GLT-1) prevented export of GLT-1 from the endoplasmic re
26 T-1; however, it did induce trafficking of a GLT-1 chimera containing the carboxyl-terminal domain of
27 on of both GluA1 and GluA2 without affecting GLT-1 expression while GLT-1 knockdown had no effect.
28 regulates GLAST expression without affecting GLT-1, as demonstrated in vitro by treatment with JAK in
30 o glutamate transporters, GLAST (EAAT-1) and GLT-1 (EAAT-2), were studied by immunohistochemistry and
34 have been identified in rat brain; GLAST and GLT-1 are primarily astrocytic, whereas EAAC1 and EAAT4
35 The glial glutamate transporters GLAST and GLT-1 are primarily responsible for the removal of gluta
37 study compares the distribution of GLAST and GLT-1 expression in the circumventricular organs of the
40 subcellular expression profile of GLAST and GLT-1 in the developing postnatal mouse hippocampus by u
42 t the glial glutamate transporters GLAST and GLT-1 limit the activation of Purkinje cell AMPA recepto
43 nsport in cultures expressing both GLAST and GLT-1, suggesting a weaker effect at GLT-1 than at GLAST
44 ressed the two glial transporters, GLAST and GLT-1, while none of the cultures expressed the neuronal
45 - to 4-times increase in levels of GLAST and GLT-1-mRNA expression both before and after scratch inju
46 rter EAAC1 in basal layer keratinocytes, and GLT-1, a related transporter, was expressed suprabasally
48 the antibiotic ceftriaxone restores xCT and GLT-1 expression following cocaine self-administration a
49 ort important and distinct roles for xCT and GLT-1 in the actions of ceftriaxone and add to a body of
50 ses the probability that mitochondria appose GLT-1 particles within astrocyte processes, without chan
54 nist of GPR30, and GPR30 siRNA on astrocytic GLT-1 expression, as well as glutamate uptake in rat pri
58 egion of DNA surrounding the GLT-1 gene (BAC GLT-1 eGFP mice) were used to assess the role of nuclear
60 everal recombinant chimeric proteins between GLT-1 and EAAC1 transporter subtypes were generated to i
61 allel fibres, knocking out GLAST or blocking GLT-1 in the absence of GLAST greatly prolonged and enha
63 lencing GPR30 reduced the expression of both GLT-1 and TGF-alpha and abrogated the G1-induced increas
64 at ceftriaxone restores the function of both GLT-1 and xCT (glutamate reuptake and export, respective
65 unocytochemical staining indicates that both GLT-1 and GLAST protein are expressed in the tanycyte po
67 lf of those observed in cortical tissue, but GLT-1 protein was present at very low levels compared wi
68 l accumulation of glutamate by GLAST than by GLT-1 cannot be used to explain the high glutamate conce
70 tate or glutamate killed the neurons, caused GLT-1 protein to decrease, and caused GLAST protein to i
72 does not alter levels of ALDH1L1, connexins, GLT-1 or binding partners of DISC1 and SR, LIS1 or PICK1
77 e (PMA) quickly and preferentially decreases GLT-1 localization on the process membrane, leading to d
79 we used an antisense strategy to knock down GLT-1 or xCT in the nucleus accumbens core and examined
83 ination of this serine did not impair either GLT-1 ubiquitination or endocytosis in response to phorb
88 port by GLAST was found to be driven, as for GLT-1, by the cotransport of 3 Na+ and 1 H+ and the coun
89 mal, control and MS white matter, except for GLT-1, which showed low-level expression around active M
91 le immunohistochemical staining patterns for GLT-1 were obtained with antibodies directed against bot
93 ntified, named EAAT1-5 in humans, and GLAST, GLT-1, EAAC1, EAAT4, and EAAT5 in rodents, respectively.
94 n (glutaminase), glutamate transport (GLAST, GLT-1 and EAAT-1), glutamate metabolism (glutamate dehyd
95 electrogenic glutamate transporters, GLAST, GLT-1, and EAAC-1, was quantitated by the reverse transc
96 of its 31 amino acid residues from the glial GLT-1 transporter was individually mutated to cysteine.
98 evaluated the functional role of the glial (GLT-1) and neuronal (EAAC1) glutamate transporters in me
100 corporation of (32)P into immunoprecipitable GLT-1, mutation of serine 486 did not reduce this signal
103 treatment elicits a significant decrease in GLT-1 activity that is prevented by preexposure to eithe
106 PPF restored the cocaine-induced decrease in GLT-1 in the accumbens core; then, using an antisense st
108 nerve transection resulted in an increase in GLT-1 compared with the control eye (P = 0.01, paired t-
113 emistry also confirmed a marked reduction in GLT-1 immunoreactivity in the cortex and hippocampus.
120 ytes with a semipermeable membrane increased GLT-1 protein, indicating that the effect of neurons was
121 ramatic change in cell morphology, increased GLT-1 and GLAST mRNA levels approximately 5-fold, increa
123 monstrate that activation of GPR30 increases GLT-1 expression via multiple pathways, suggesting that
133 cient mice infected with NSV exhibit neither GLT-1 downregulation nor neuronal death of brainstem and
134 n expected, and the contribution of neuronal GLT-1 to synaptosomal glutamate uptake is greater than e
135 of dihydrokainate, suggesting that neuronal GLT-1 is capable of participating in the clearance of sy
136 e-labeling experiments suggest that neuronal GLT-1 protein is primarily localized to the dendrites of
137 tamate escape into the surrounding neuropil, GLT-1 preserves the spatial specificity of synaptic sign
139 hysiological conditions approximately 35% of GLT-1 transporters function as buffers, releasing glutam
142 tes resulted in loss of approximately 80% of GLT-1 protein and of glutamate uptake activity that coul
143 eras containing the first 446 amino acids of GLT-1 were not functional unless amino acids 475-517 of
144 ther, these studies suggest that blockade of GLT-1 in the CEA is sufficient to induce both anhedonia
145 ly, we demonstrated that central blockade of GLT-1 induces anhedonia and c-Fos expression in the PFC.
146 t the initially proposed characterization of GLT-1 as a purely glial transporter is too simplistic an
149 a containing the carboxyl-terminal domain of GLT-1; however, it did induce trafficking of a GLT-1 chi
152 n reported that the regulated endocytosis of GLT-1 depends on its ubiquitination triggered by protein
153 to alanine (6L/6A GLT-1) prevented export of GLT-1 from the endoplasmic reticulum (ER) to the plasma
154 used antisense to decrease the expression of GLT-1 and xCT (a catalytic subunit of Sxc) to determine
163 the effect of neurons on glial expression of GLT-1 protein, but the addition of dbcAMP to mixed cultu
164 gh neurons activate astrocytic expression of GLT-1, the mechanisms involved have not been identified.
165 ytes with neurons also induced expression of GLT-1, which colocalized with the glial specific marker,
168 Nedd4-2 phosphorylation and the formation of GLT-1.Nedd4-2 complexes, whereas siRNA knockdown of Nedd
171 neuron-conditioned medium, the induction of GLT-1 by neuron-conditioned medium was completely abolis
174 nal cultures contribute to this induction of GLT-1, but little is known about the signaling pathways
176 lts support the idea that enhanced levels of GLT-1 in transgenic mice are responsible for reducing H/
179 st that greater oxidative stress and loss of GLT-1 function selectively in CA1 astrocytes is central
180 is additional mutation rescued maturation of GLT-1 essentially excludes the possibility that the 6L/6
181 atment, suggesting that the morphogenesis of GLT-1 clusters is highly dependent on the actin network.
187 sms that mediate TX-induced up-regulation of GLT-1 (EAAT2 in humans), we investigated its effect on G
188 tance of these clusters in the regulation of GLT-1 activity in the presence or absence of neurons.
190 e differential and subregional regulation of GLT-1 isoforms in neuronal and glial compartments in the
202 studies demonstrate a novel effect of PKC on GLT-1 activity and define a unique carboxyl-terminal dom
205 Chimeras consisting of domains from EAAC1 or GLT-1 were used to investigate structural motifs involve
206 appaB subunits induced expression of eGFP or GLT-1 and increased GLT-1-mediated transport activity.
207 ng the glial glutamate transporters GLAST or GLT-1, the ischaemia-evoked AD current was indistinguish
208 hexokinase-1 overlapped with mitochondria or GLT-1, strongly suggesting that GLT-1, mitochondria, and
210 the distal end of C6 glioma cell processes, GLT-1 clusters undergo rapid morphological changes in bo
211 te the ability of endogenous and recombinant GLT-1 to form clusters in astrocytic processes and chara
214 analysis demonstrated significantly reduced GLT-1 in glaucomatous eyes compared with control eyes at
215 F during the first week after stroke reduced GLT-1 upregulation as well as long-term behavioral recov
216 synaptically released glutamate by reducing GLT-1 surface expression in mouse astrocytes and that th
219 This suggests that neurons do not regulate GLT-1 by activation of PKA but that neurons and dbcAMP r
222 ingly, a high percentage of variably spliced GLT-1 mRNAs lacking parts of this domain are found in th
225 DAR 1]) and a glutamate transporter subtype [GLT-1] within the leech CNS using mono- and polyclonal a
226 ced hippocampal slices, fluorescently tagged GLT-1 puncta overlapped with fluorescently tagged mitoch
227 ther adult brain areas at a lower level than GLT-1, and is present throughout the brain early in deve
229 anxiety and depression, we hypothesized that GLT-1 blockade in the CEA would induce symptoms of anhed
230 PFC in regulating mood, we hypothesized that GLT-1 blockade in the PFC alone would be sufficient to i
233 th previous results, these studies show that GLT-1 cocompartmentalizes with Na(+)/K(+) ATPase, glycol
236 ochondria or GLT-1, strongly suggesting that GLT-1, mitochondria, and the first step in glycolysis ar
238 when GLT-1 was deleted in neurons, both the GLT-1 protein and glutamate uptake activity that could b
247 cell surface expression and activity of the GLT-1 subtype of glutamate transporter were examined in
249 analyses revealed a robust expression of the GLT-1 transporter protein in the SON, which was diminish
250 , -583/-282/-251) or CRE (-308) sites on the GLT-1 promoter led to significant repression of the prom
251 g a very large region of DNA surrounding the GLT-1 gene (BAC GLT-1 eGFP mice) were used to assess the
252 d uptake to dihydrokainate suggests that the GLT-1 (glutamate transporter-1) subtype primarily mediat
257 activity for the third glutamate transporter GLT-1 (EAAT2), a putatively glial transporter, in microc
258 sion of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease me
260 regulation of the glia glutamate transporter GLT-1 and the recently identified GLT isoform, GLT-1b, i
261 sion of the astrocytic glutamate transporter GLT-1 and to attenuated changes in dendrite morphology,
262 vels of the astrocytic glutamate transporter GLT-1 but normal expression levels of another glial glut
264 al inhibition of glial glutamate transporter GLT-1 induced the similar Kv2.1 dephosphorylation, where
266 or GFAP, S100beta, and glutamate transporter GLT-1 within a few hours of reperfusion, but without ast
267 inhibitor of the glial glutamate transporter GLT-1, did not block the increase in glutamate uptake.
268 sense strategy against glutamate transporter GLT-1, we found that restored transporter expression was
269 ade of the astrocytic glutamate transporter (GLT-1) induces anhedonia and c-Fos expression in areas t
271 airment of astrocytic glutamate transporter (GLT-1; EAAT2) function is associated with multiple neuro
274 of the most abundant glutamate transporter, GLT-1, predicts that a very low glutamate concentration,
275 l levels of the glial glutamate transporter, GLT-1, were higher in brains of transgenic as compared t
278 n expression of glutamate (Glu) transporters GLT-1 and GLAST and attenuated Glu uptake (p < 0.01).
279 A and protein for the glutamate transporters GLT-1 and GLAST in unique tanycyte populations of the th
280 pression of the glial glutamate transporters GLT-1 and GLAST was studied in primary cultures derived
281 d that the astroglial glutamate transporters GLT-1 and GLAST, but not the neuronal transporter EAAC1,
284 ective dominant-negative effect on wild-type GLT-1 expression and formed coimmunoprecipitable complex
286 e not blocked by PKA antagonists, but unlike GLT-1, the addition of dbcAMP to mixed cultures of neuro
287 evealed that ceftriaxone does not upregulate GLT-1 and xCT through a transcriptional mechanism, and t
288 pse, nor is it clear whether the upregulated GLT-1 is functionally important for suppressing of drug
289 enuating reinstatement and from upregulating GLT-1 and resulted in increased surface expression of AM
292 by pituicytes in the posterior lobe, whereas GLT-1 is expressed only by the astrocyte-like cells in t
293 rocytic cells near the pineal stalk, whereas GLT-1 is expressed by pinealocytes throughout the gland.
295 ic extracellular glutamate in the NAc, while GLT-1 is responsible for the majority of glutamate uptak
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