ライフサイエンスコーパス: EAAT3

1 or EAAC1 (for excitatory amino acid carrier; EAAT3).

2 e of a human neuronal glutamate transporter (EAAT3).

3 on astrocytes (EAAT1 and EAAT2) and neurons (EAAT3).

4 by the human neuronal glutamate transporter EAAT3.

5 dependent excitatory amino acid transporter, EAAT3.

6 acid transporter subtypes EAAT1, EAAT2, and EAAT3.

7 mice genetically deficient in either Nrf2 or EAAT3.

8 t to locate the third sodium-binding site in EAAT3.

9 l-length coding regions of EAAT1, EAAT2, and EAAT3.

10 ine did not affect the isoflurane effects on EAAT3.

11 and also abolished the isoflurane effects on EAAT3.

12 redistribution and a direct effect of PKC on EAAT3.

13 ique sequence in the cytosolic C terminus of EAAT3.

14 a-helices) suggested an oligomeric state for EAAT3.

15 ly used anesthetic, enhanced the activity of EAAT3, a major neuronal EAAT.

16 the promoter region of the gene encoding for EAAT3, a neuronal EAAT, but not in the promoter regions

17 le of serine 465 in the isoflurane-increased EAAT3 activity and redistribution and a direct effect of

18 in EAAT3 by PKCalpha mediates the increased EAAT3 activity and redistribution to plasma membrane aft

19 ine abolished isoflurane-induced increase of EAAT3 activity and redistribution to the plasma membrane

20 through excitatory amino acid transporter 3 [EAAT3; also termed Slc1a1 (solute carrier family 1 membe

21 Consistent with this decrease in surface EAAT3, amphetamine potentiates excitatory synaptic respo

22 ent labeling and inactivation correlation on EAAT3 and EAAT4 to determine whether the glutamate-activ

23 rent by glutamate is approximately 1 in both EAAT3 and EAAT4.

24 ced hippocampal levels of neuropeptide Y and EAAT3 and increased calpain proteolysis of alphaII spect

25 neuronal damage, and compensatory changes in EAAT3 and neuropeptide Y.

26 f this residue in different conformations of EAAT3 and with different ligands bound.

27 ) express two glutamate transporters, EAAC1 (EAAT3) and EAAT4; however, their relative contribution t

28 al EAAT2 and a minor portion of total EAAT1, EAAT3, and EAAT4 were associated with lipid rafts.

29 een identified in human brain: EAAT1, EAAT2, EAAT3, and EAAT4.

30 phosphorylation of wild type, T5A, and T498A EAAT3, and this increase was absent in S465A and S465D.

31 three transporters, GLAST (EAAT1) and EAAC1 (EAAT3), are localized to microculture glia and neurons,

32 higher affinity for the neuronal transporter EAAT3 as a result of a slower dissociation rate.

33 euronal excitatory amino acid transporter 3 (EAAT3) blocks potentiation, suggesting that EAAT3 intern

34 o observed in neuronal glutamate transporter EAAT3 but to a lesser extent.

35 significantly different for EAAT1, EAAT2, or EAAT3, but 2-FAA exhibited higher affinity for the neuro

36 st that the phosphorylation of serine 465 in EAAT3 by PKCalpha mediates the increased EAAT3 activity

37 ulation of the neuronal cysteine transporter EAAT3 by the Nrf2-ARE pathway.

38 ion assays demonstrated that deletion of the EAAT3 C terminus or replacement of the C terminus of EAA

39 AT2 (kainic acid and dihydrokainic acid) and EAAT3 (cysteine).

40 h-affinity excitatory amino acid transporter EAAT3 (EAAC1) facilitates glutamate uptake into most cel

41 eine was transported by the neuronal subtype EAAT3 (EAAC1) with an affinity constant of 190 microM an

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

43 EAAT3 (excitatory amino acid transporter type 3, the neu

44 We showed that RFX1 increased EAAT3 expression and activity in C6 glioma cells.

45 by RFX1 antisense oligonucleotides decreased EAAT3 expression in rat cortical neurons in culture.

46 ugh transcriptional upregulation of neuronal EAAT3 expression.

47 appeared in the protoplasmic face only after EAAT3 expression.

48 age-, and substrate-dependent alterations of EAAT3 fluorescence intensities.

49 in that functions as a negative regulator of EAAT3 function.

50 In this study, we use an EAAT3 homology model to calculate the pKa of several tit

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

52 titative change in mRNA for EAAT1, EAAT2, or EAAT3 in ALS motor cortex, even in patients with a large

53 sequence also impairs dendritic targeting of EAAT3 in hippocampal neurons but does not interfere with

54 fundamental features of the localization of EAAT3 in neurons, its restriction to the somatodendritic

55 The cross-sectional area of EAAT3 in the plasma membrane (48 +/- 5 nm(2)) predicted

56 to aspartic acid increased the expression of EAAT3 in the plasma membrane and also abolished the isof

57 ed that this particle represented functional EAAT3 in the plasma membrane.

58 sis of an excitatory amino acid transporter, EAAT3, in dopamine neurons.

59 Recently, a novel rat EAAT3-interacting protein called GTRAP3-18 has been iden

60 neurons blocks the effects of amphetamine on EAAT3 internalization and its action on excitatory respo

61 (EAAT3) blocks potentiation, suggesting that EAAT3 internalization increases extracellular glutamate

62 PH-101 and UCPH-102 for EAAT1 over EAAT2 and EAAT3 is demonstrated to extend to the EAAT4 and EAAT5 s

63 sporter excitatory amino acid transporter 3 (EAAT3) is polarized to the apical surface in epithelial

64 he human transporter clones EAAT1, EAAT2, or EAAT3, it was found that the pharmacological profile of

65 thway in mouse brain increased both neuronal EAAT3 levels and neuronal glutathione content, and these

66 The linear correlation between EAAT3 maximum carrier-mediated charge and the total numb

67 Mouse GTRAP3-18 inhibited EAAT3-mediated glutamate transport in a dose-dependent m

68 RAP3-18 functions as a negative modulator of EAAT3-mediated glutamate transport.

69 ed significantly from that of both EAAT1 and EAAT3 mRNA.

70 and hypertrophied hearts expressed EAAT1 and EAAT3 mRNA.

71 th IC(50) values for inhibition of EAAT1 and EAAT3 of 5 and 3.8 microM, respectively, corresponding t

72 The pentameric structure of EAAT3 offers new insights into its function as both a gl

73 ut does not interfere with the clustering of EAAT3 on dendritic spines and filopodia.

74 led the presence of a member of this family, EAAT3, on the erythrocyte membrane.

75 Inhibition of EAAT3 or sodium-free buffer conditions prevented accumul

76 EAAT3 particles were pentagonal in shape in which five d

77 The activity of EAAT3 promoter as measured by luciferase reporter activi

78 served ARE-related sequence was found in the EAAT3 promoter of several mammalian species.

79 s suggest that RFX1 enhances the activity of EAAT3 promoter to increase the expression of EAAT3 prote

80 r was sufficient to upregulate both neuronal EAAT3 protein and glutathione content.

81 EAAT3 protein expression in isolated cells and vesicles

82 EAAT3 protein expression was significantly greater in ce

83 mmunoblot analysis confirmed the presence of EAAT3 protein, however, we were unable to detect EAAT1 p

84 EAAT3 promoter to increase the expression of EAAT3 proteins.

85 red a protein kinase C (PKC) alpha-dependent EAAT3 redistribution to the plasma membrane.

86 h a 14- and 9-fold preference over EAAT2 and EAAT3, respectively.

87 g 30- and 50-fold selectivity over EAAT1 and EAAT3, respectively.

88 be approximately 1:3:6 for EAAT1, EAAT2, and EAAT3, respectively.

89 appears to be mediated predominantly by the EAAT3 subtype.

90 of wild-type neuronal glutamate transporter EAAT3 subunits with subunits mutated at R447, a residue

91 ent of PKCalpha in the isoflurane effects on EAAT3, suggest that the phosphorylation of serine 465 in

92 In this study, we analyzed the sequences in EAAT3 that are responsible for its polarized localizatio

93 otif in the cytoplasmic C-terminal region of EAAT3 that directs its apical localization in MDCK cells

94 vators and Nrf2 overexpression both produced EAAT3 transcriptional activation in C6 cells.

95 Because the EAAT3 transporter is also expressed in tissues including

96 Transcripts for both the EAAT1 and EAAT3 transporter subtypes were detected but not for EAA

97 energy transfer on oocytes expressing mutant EAAT3 transporters to determine the location and functio

98 se data indicate that the internalization of EAAT3 triggered by amphetamine increases glutamatergic s

99 EAAT3 was expressed in Xenopus laevis oocytes, and its f

100 cDNA for EAAT1, EAAT2, and EAAT3 was observed, indicating that mRNA was present.

101 id transporter transcripts EAAT1, EAAT2, and EAAT3 was performed in discrete thalamic nuclei in perso

102 The C terminus of EAAT3 was sufficient to redirect the basolateral-preferr

103 orms of GltPh as well on a homology model of EAAT3, we sought to locate the third sodium-binding site

104 ranscripts encoding EAAT1 and EAAT2, but not EAAT3, were detected in the thalamus of subjects with sc

105 dy, we prepared COS7 cells stably expressing EAAT3 with or without mutations of potential PKC phospho

106 terminus or replacement of the C terminus of EAAT3 with the analogous region in EAAT1 eliminated apic