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1 f human excitatory amino acid transporter 3 (EAAT3)).
2 e of a human neuronal glutamate transporter (EAAT3).
3 on astrocytes (EAAT1 and EAAT2) and neurons (EAAT3).
4 or EAAC1 (for excitatory amino acid carrier; EAAT3).
5  by the human neuronal glutamate transporter EAAT3.
6  acid transporter subtypes EAAT1, EAAT2, and EAAT3.
7 ique sequence in the cytosolic C terminus of EAAT3.
8 dependent excitatory amino acid transporter, EAAT3.
9 mice genetically deficient in either Nrf2 or EAAT3.
10 t to locate the third sodium-binding site in EAAT3.
11 l-length coding regions of EAAT1, EAAT2, and EAAT3.
12 ine did not affect the isoflurane effects on EAAT3.
13 and also abolished the isoflurane effects on EAAT3.
14 redistribution and a direct effect of PKC on EAAT3.
15 a-helices) suggested an oligomeric state for EAAT3.
16 ly used anesthetic, enhanced the activity of EAAT3, a major neuronal EAAT.
17 the promoter region of the gene encoding for EAAT3, a neuronal EAAT, but not in the promoter regions
18 le of serine 465 in the isoflurane-increased EAAT3 activity and redistribution and a direct effect of
19  in EAAT3 by PKCalpha mediates the increased EAAT3 activity and redistribution to plasma membrane aft
20 ine abolished isoflurane-induced increase of EAAT3 activity and redistribution to the plasma membrane
21                  Recent studies suggest that EAAT3 also transports the oncometabolite R-2-hydroxyglut
22 through excitatory amino acid transporter 3 [EAAT3; also termed Slc1a1 (solute carrier family 1 membe
23     Consistent with this decrease in surface EAAT3, amphetamine potentiates excitatory synaptic respo
24 ent labeling and inactivation correlation on EAAT3 and EAAT4 to determine whether the glutamate-activ
25 rent by glutamate is approximately 1 in both EAAT3 and EAAT4.
26 ced hippocampal levels of neuropeptide Y and EAAT3 and increased calpain proteolysis of alphaII spect
27 neuronal damage, and compensatory changes in EAAT3 and neuropeptide Y.
28 f this residue in different conformations of EAAT3 and with different ligands bound.
29 ) express two glutamate transporters, EAAC1 (EAAT3) and EAAT4; however, their relative contribution t
30 euronal excitatory amino acid transporter 3 (EAAT3) and enzymatic conversion of glutamate to GABA.
31 al EAAT2 and a minor portion of total EAAT1, EAAT3, and EAAT4 were associated with lipid rafts.
32 een identified in human brain: EAAT1, EAAT2, EAAT3, and EAAT4.
33 phosphorylation of wild type, T5A, and T498A EAAT3, and this increase was absent in S465A and S465D.
34 three transporters, GLAST (EAAT1) and EAAC1 (EAAT3), are localized to microculture glia and neurons,
35 higher affinity for the neuronal transporter EAAT3 as a result of a slower dissociation rate.
36 (R)-7 [(R)-AS-1] was not active in EAAT1 and EAAT3 assays and did not show significant off-target act
37 euronal excitatory amino acid transporter 3 (EAAT3) blocks potentiation, suggesting that EAAT3 intern
38  electron microscopy (cryo-EM) structures of EAAT3 bound to different substrates.
39                                   Imaging of EAAT3 bound to L-cysteine revealed several conformationa
40  high-resolution cryo-EM structures of human EAAT3 bound to the neurotransmitter glutamate with sympo
41 o observed in neuronal glutamate transporter EAAT3 but to a lesser extent.
42 significantly different for EAAT1, EAAT2, or EAAT3, but 2-FAA exhibited higher affinity for the neuro
43 st that the phosphorylation of serine 465 in EAAT3 by PKCalpha mediates the increased EAAT3 activity
44 ulation of the neuronal cysteine transporter EAAT3 by the Nrf2-ARE pathway.
45 ion assays demonstrated that deletion of the EAAT3 C terminus or replacement of the C terminus of EAA
46 AT2 (kainic acid and dihydrokainic acid) and EAAT3 (cysteine).
47 h-affinity excitatory amino acid transporter EAAT3 (EAAC1) facilitates glutamate uptake into most cel
48 eine was transported by the neuronal subtype EAAT3 (EAAC1) with an affinity constant of 190 microM an
49 tissue: GLAST (EAAT1), GLT-1 (EAAT2), EAAC1 (EAAT3), EAAT4, and EAAT5.
50                                              EAAT3 (excitatory amino acid transporter type 3, the neu
51                We showed that RFX1 increased EAAT3 expression and activity in C6 glioma cells.
52 nd evaluated the overall impact of increased EAAT3 expression at behavioral and synaptic levels.
53 by RFX1 antisense oligonucleotides decreased EAAT3 expression in rat cortical neurons in culture.
54 ugh transcriptional upregulation of neuronal EAAT3 expression.
55 appeared in the protoplasmic face only after EAAT3 expression.
56 age-, and substrate-dependent alterations of EAAT3 fluorescence intensities.
57 hesis of OCD, particularly for the increased EAAT3 function, and provide a valuable animal model that
58 in that functions as a negative regulator of EAAT3 function.
59       We generated a transgenic mouse model (EAAT3(glo)) to achieve conditional, Cre-dependent EAAT3
60                                              EAAT3(glo)/CMKII mice also displayed greater spontaneous
61 ical analyses at corticostriatal synapses of EAAT3(glo)/CMKII mice revealed changes in NMDA receptor
62 erexpression driven by CaMKIIalpha-promoter (EAAT3(glo)/CMKII) displayed increased anxiety-like and r
63  encoding the neuronal glutamate transporter EAAT3 has been proposed as a candidate gene for this dis
64 eral mouse models fully or partially lacking EAAT3 have shown no alterations in baseline anxiety-like
65                     In this study, we use an EAAT3 homology model to calculate the pKa of several tit
66 at EAAT1 (IC50 20 muM) compared to EAAT2 and EAAT3 (IC50 > 300 muM).
67                                              EAAT3 immunoreactivity was strongly localized to presump
68 titative change in mRNA for EAAT1, EAAT2, or EAAT3 in ALS motor cortex, even in patients with a large
69 sequence also impairs dendritic targeting of EAAT3 in hippocampal neurons but does not interfere with
70  fundamental features of the localization of EAAT3 in neurons, its restriction to the somatodendritic
71                  The cross-sectional area of EAAT3 in the plasma membrane (48 +/- 5 nm(2)) predicted
72 to aspartic acid increased the expression of EAAT3 in the plasma membrane and also abolished the isof
73 ed that this particle represented functional EAAT3 in the plasma membrane.
74            We found that L-cysteine binds to EAAT3 in thiolate form, and EAAT3 recognizes different s
75 sis of an excitatory amino acid transporter, EAAT3, in dopamine neurons.
76                        Recently, a novel rat EAAT3-interacting protein called GTRAP3-18 has been iden
77 neurons blocks the effects of amphetamine on EAAT3 internalization and its action on excitatory respo
78 (EAAT3) blocks potentiation, suggesting that EAAT3 internalization increases extracellular glutamate
79 PH-101 and UCPH-102 for EAAT1 over EAAT2 and EAAT3 is demonstrated to extend to the EAAT4 and EAAT5 s
80                            Among five EAATs, EAAT3 is the only isoform that can efficiently transport
81 sporter excitatory amino acid transporter 3 (EAAT3) is polarized to the apical surface in epithelial
82 Asp) and glutamate (Glu) transporter, SLC1A1/EAAT3, is a metabolic dependency in ccRCC.
83 he human transporter clones EAAT1, EAAT2, or EAAT3, it was found that the pharmacological profile of
84 thway in mouse brain increased both neuronal EAAT3 levels and neuronal glutathione content, and these
85               The linear correlation between EAAT3 maximum carrier-mediated charge and the total numb
86                    Mouse GTRAP3-18 inhibited EAAT3-mediated glutamate transport in a dose-dependent m
87 RAP3-18 functions as a negative modulator of EAAT3-mediated glutamate transport.
88 ed significantly from that of both EAAT1 and EAAT3 mRNA.
89 and hypertrophied hearts expressed EAAT1 and EAAT3 mRNA.
90 th IC(50) values for inhibition of EAAT1 and EAAT3 of 5 and 3.8 microM, respectively, corresponding t
91                  The pentameric structure of EAAT3 offers new insights into its function as both a gl
92 ut does not interfere with the clustering of EAAT3 on dendritic spines and filopodia.
93 led the presence of a member of this family, EAAT3, on the erythrocyte membrane.
94                                Inhibition of EAAT3 or sodium-free buffer conditions prevented accumul
95 (glo)) to achieve conditional, Cre-dependent EAAT3 overexpression and evaluated the overall impact of
96                                    Mice with EAAT3 overexpression driven by CaMKIIalpha-promoter (EAA
97                                              EAAT3 particles were pentagonal in shape in which five d
98                              The activity of EAAT3 promoter as measured by luciferase reporter activi
99 served ARE-related sequence was found in the EAAT3 promoter of several mammalian species.
100 s suggest that RFX1 enhances the activity of EAAT3 promoter to increase the expression of EAAT3 prote
101 r was sufficient to upregulate both neuronal EAAT3 protein and glutathione content.
102                                              EAAT3 protein expression in isolated cells and vesicles
103                                              EAAT3 protein expression was significantly greater in ce
104 mmunoblot analysis confirmed the presence of EAAT3 protein, however, we were unable to detect EAAT1 p
105 EAAT3 promoter to increase the expression of EAAT3 proteins.
106 ysteine binds to EAAT3 in thiolate form, and EAAT3 recognizes different substrates by fine-tuning loc
107 red a protein kinase C (PKC) alpha-dependent EAAT3 redistribution to the plasma membrane.
108 be approximately 1:3:6 for EAAT1, EAAT2, and EAAT3, respectively.
109 h a 14- and 9-fold preference over EAAT2 and EAAT3, respectively.
110 g 30- and 50-fold selectivity over EAAT1 and EAAT3, respectively.
111  appears to be mediated predominantly by the EAAT3 subtype.
112  of wild-type neuronal glutamate transporter EAAT3 subunits with subunits mutated at R447, a residue
113 ent of PKCalpha in the isoflurane effects on EAAT3, suggest that the phosphorylation of serine 465 in
114  In this study, we analyzed the sequences in EAAT3 that are responsible for its polarized localizatio
115 otif in the cytoplasmic C-terminal region of EAAT3 that directs its apical localization in MDCK cells
116 vators and Nrf2 overexpression both produced EAAT3 transcriptional activation in C6 cells.
117                                  Because the EAAT3 transporter is also expressed in tissues including
118           Transcripts for both the EAAT1 and EAAT3 transporter subtypes were detected but not for EAA
119 energy transfer on oocytes expressing mutant EAAT3 transporters to determine the location and functio
120 se data indicate that the internalization of EAAT3 triggered by amphetamine increases glutamatergic s
121                                              EAAT3 was expressed in Xenopus laevis oocytes, and its f
122                   cDNA for EAAT1, EAAT2, and EAAT3 was observed, indicating that mRNA was present.
123 id transporter transcripts EAAT1, EAAT2, and EAAT3 was performed in discrete thalamic nuclei in perso
124                            The C terminus of EAAT3 was sufficient to redirect the basolateral-preferr
125                However, using purified human EAAT3, we could not observe R-2HG binding or transport.
126 orms of GltPh as well on a homology model of EAAT3, we sought to locate the third sodium-binding site
127 ranscripts encoding EAAT1 and EAAT2, but not EAAT3, were detected in the thalamus of subjects with sc
128 dy, we prepared COS7 cells stably expressing EAAT3 with or without mutations of potential PKC phospho
129 terminus or replacement of the C terminus of EAAT3 with the analogous region in EAAT1 eliminated apic

 
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