ライフサイエンスコーパス: EAAT

1 EAAT anion channels regulate neuronal excitability, and

2 EAAT inactivity also results in elevated internalization

3 EAAT-2 expression was inversely correlated with tumor gr

4 EAATs also mediate a thermodynamically uncoupled substra

5 EAATs also mediate a thermodynamically uncoupled substra

6 EAATs are glutamate transporters and anion-selective ion

7 EAATs are not only secondary active glutamate transporte

8 EAATs are trimeric proteins and are thought to comprise

9 EAATs reside on rod bipolar cell axon terminals where GA

10 mate transporters, GLAST (EAAT-1) and GLT-1 (EAAT-2), were studied by immunohistochemistry and quanti

11 creased excitatory amino acid transporter-2 (EAAT-2) expression in high-grade glial tumors compared w

12 Because of abundant EAAT expression, glutamate clearance from the extracellu

13 on of tumor growth at sites that received Ad-EAAT-2-infected cells.

14 d caspase-3 activation all indicated that Ad-EAAT-2 infection elicited apoptosis in glioma cells.

15 Infection of glioma cells with Ad-EAAT-2 resulted in a physiologic level of functional EAA

16 s response is inhibited by the high-affinity EAAT antagonist TBOA (dl-threo-beta-benzyloxyaspartic ac

17 useful to screen novel EAAT ligands for all EAAT subtypes.

18 system to characterize EAAT ligands for all EAAT subtypes.

19 erimental manipulations resulting in altered EAAT expression, our findings show that astrocytic gluta

20 Glutamate also evokes an EAAT-mediated Cl(-) current, but its role in CNS signali

21 mediated independently by each subunit of an EAAT multimer.

22 nase), glutamate transport (GLAST, GLT-1 and EAAT-1), glutamate metabolism (glutamate dehydrogenase [

23 Although crosstalk between the receptors and EAATs is conceivable, whether and how the transporter ac

24 Several crystal structures of an archaeal EAAT homolog, GltPh, at different stages of the transpor

25 In the model system Glt(Ph), an archaeal EAAT homologue from Pyrococcus horikoshii, limited tryps

26 GltPh, an archeal EAAT homolog from Pyrococcus horikoshii, is currently th

27 reasing intracellular glutamate via blocking EAAT-3, mimics the effects of intracellular mGluR5 antag

28 ansport and anion channel properties of both EAAT isoforms.

29 , and both responses were again abolished by EAAT and NCX blockers.

30 reover, these responses were counteracted by EAAT and NCX blockers, as observed in SH-SY5Y and C6 cel

31 ctrogenic, postsynaptic currents mediated by EAATs should permit precise calculation of the amount of

32 llular glutamate and its local regulation by EAATs.

33 ported that they blocked glutamate uptake by EAATs 1-5 much more potently than TBOA.

34 loped a binding assay system to characterize EAAT ligands for all EAAT subtypes.

35 Recent progress has seen the use of cloned EAAT subtypes to develop transporter inhibitors with imp

36 operties of (S)-glutamate or the competitive EAAT inhibitor TBOA significantly.

37 signals, we postulate that presynaptic cone EAATs contribute to the encoding of contrast sensitivity

38 so function as anion channels, and different EAATs vary considerably in glutamate transport rates and

39 In the salamander retina, five distinct EAAT-encoding genes have been cloned, making the amphibi

40 Asp analogues provide analogues with diverse EAAT subtype selectivity profiles.

41 e responsible for the observed effect during EAAT suppression.

42 T-transfected COS-1 cell membranes with each EAAT subtype.

43 Pharmacological inhibition of either EAAT or NCX counteracted the Glu-induced ATP synthesis.

44 Since EAAT2 is the most expressed EAAT in the nTS, this study specifically determined EAAT

45 H9c2 expresses EAATs but lacks endogenous NCX1 expression.

46 n voltage-clamped Xenopus oocytes expressing EAATs and used concentration jumps to measure binding an

47 ansporter subtypes were detected but not for EAATs 2, 4, and 5.

48 esulted in a physiologic level of functional EAAT-2, and a subsequent dose-dependent reduction in cel

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

50 carriers, predominantly involving the glial EAAT 2 transporter.

51 fic contributions made by neuronal and glial EAATs have not been determined.

52 enes encoding for EAAT1 and EAAT2, two glial EAATs.

53 e affinity for the transported amino acid in EAATs.

54 ich substrates gate the anion conductance in EAATs and suggest that in EAAT1, Arg-388 is a critical e

55 ce of induced fit for substrate selection in EAATs and illustrate how high-affinity binding and the e

56 statement of CPP and significantly increased EAAT(2) mRNA levels in the mPFC, with a trend towards si

57 ptosomal uptake with those of the individual EAAT clones.

58 ltPh and patch-clamp recordings of mammalian EAATs to determine how these transporters conduct anions

59 In transmembrane domain 4, the mammalian EAATs contain a stretch of over 50 amino acids (4B-4C lo

60 ely, these data suggest that plasma membrane EAAT and NCX are both involved in Glu-induced ATP synthe

61 al activity rapidly and reversibly modulates EAAT-dependent glutamate transport.

62 n of the gene encoding for EAAT3, a neuronal EAAT, but not in the promoter regions of the genes encod

63 nced the activity of EAAT3, a major neuronal EAAT.

64 is rapidly bound and inactivated by neuronal EAATs located on postsynaptic PCs.

65 By subtracting this residual non-EAAT current from the response recorded in glutamate rec

66 binding assay will be useful to screen novel EAAT ligands for all EAAT subtypes.

67 high Hill coefficients for the activation of EAAT anion currents by glutamate and suggests that the s

68 a mutual interplay between the activities of EAAT and NCX, coimmunoprecipitation studies showed a phy

69 shown to modify the substrate dependence of EAAT anion currents.

70 nsistent with glutamate spillover, effect of EAAT inhibition on AMPAR distribution and stability is d

71 divergent temporal and spatial expression of EAAT subtypes and their persistence in mature fiber trac

72 ely, our results uncovered a new function of EAAT-2 in controlling glioma proliferation.

73 Gating of EAAT anion channels is tightly coupled to transitions wi

74 ch was reflected by an undetectable level of EAAT-2 protein in glioma cell lines.

75 studies have investigated the regulation of EAAT expression.

76 We previously established the importance of EAATs in the nTS by demonstrating their inhibition produ

77 also inhibited by localised inactivation of EAATs in individual astrocytes, using internal DL-threo-

78 ntal data on substrate binding properties of EAATs.

79 We expanded our studies on EAAT/NCX interplay in the H9c2 cells.

80 Using real time PCR, EAAT(2) mRNA levels in the nucleus accumbens (NAc) and m

81 ents suggests that, on average, postsynaptic EAATs take up approximately 1,300,000 glutamate molecule

82 In addition to several potent EAAT inhibitors displaying IC50 values approximately 1 m

83 Bright light evoked predominantly EAAT-mediated inhibition with slow kinetics and a small

84 Studies probing EAAT function suggest that their capacity to remove glut

85 mate; E:xcitatory A:mino A:cid T:ransporter; EAAT).

86 t to investigate the effect of reconstituted EAAT-2 on glioma cell growth in vitro and in vivo by ade

87 d and functionally characterized two retinal EAATs from mouse, the GLT-1/EAAT2 splice variant GLT-1c,

88 cal roles of each subtype, subtype-selective EAAT ligands are required.

89 ture glutamate from the extracellular space, EAATs exhibit a sodium- and glutamate-gated anion conduc

90 and radial glia layers reveal that specific EAATs are likely to play multiple distinct roles in the

91 r, this is possible only if a stoichiometric EAAT current can be isolated from all other contaminatin

92 mphibian retina an excellent system to study EAAT function.

93 Analysis of such synaptic EAAT currents suggests that, on average, postsynaptic EA

94 Given that EAAT transporters are inhibited by low pH, other transpo

95 tly alters predictions of the influence that EAAT-mediated anion currents will have on synaptic trans

96 field but also substantiates the notion that EAAT ligands not derived from alpha-amino acids hold con

97 We show in mouse retina that EAAT-mediated Cl(-) currents that were evoked by light i

98 It has been suggested that EAAT subtypes with particularly large anion conductances

99 transport, primarily from glial cells by the EAAT 2 carrier, is responsible for a substantial (42 and

100 ently available pharmacological tools in the EAAT field but also substantiates the notion that EAAT l

101 competitive, non-transported blocker of the EAAT 1-3 transporters.

102 mportance of the trimerization domain of the EAAT and demonstrates the feasibility of modulating tran

103 AAT5 shares the structural homologies of the EAAT gene family, one novel feature of the EAAT5 sequenc

104 d light on some controversial aspects of the EAAT transport cycle, including the kinetics of proton b

105 anslocation and the gating mechanisms of the EAAT-associated anion channel.

106 test the efficacy of compounds targeting the EAAT(2) in human methamphetamine-dependent users.

107 n conductance is highly conserved within the EAAT protein family.

108 The EAATs are secondary transporters that couple the Na(+) g

109 n determining differences between ASCT1, the EAATs and GltPh.

110 Acidic amino acid transport by the EAATs is coupled to the co-transport of three Na(+) ions

111 s, ASCTs function quite differently from the EAATs and GltPh.

112 ole of clearing extracellular glutamate, the EAATs also possess a thermodynamically uncoupled Cl(-) c

113 in ASCT1 that correspond to residues in the EAATs and GltPh that are involved in Na(+) binding.

114 ransporter with functional properties of the EAATs and GltPh, to further our understanding of the str

115 ay explain the faster transport rates of the EAATs compared to its archaeal homologs.

116 nt of potent and selective inhibitors of the EAATs has contributed greatly to the understanding of th

117 ructure of GltPh, an archaeal homolog of the EAATs, provides elegant structural details of this famil

118 Thus, the EAATs in the abluminal membrane shift glutamate from the

119 In contrast to the EAATs, transport via GltPh is independent of H+ and K+.

120 ignificant high-affinity specific binding to EAAT-transfected COS-1 cell membranes with each EAAT sub

121 The switch to EAAT-mediated signaling in bright light supplements rece

122 ansporter excitatory amino acid transporter (EAAT) 1, also known as glutamate aspartate transporter (

123 neuronal excitatory amino acid transporter (EAAT) 3 glutamate transporter covalently labeled with a

124 rs of the excitatory amino acid transporter (EAAT) family of proteins that remove glutamate from the

125 ts in the excitatory amino acid transporter (EAAT) family.

126 on of the excitatory amino acid transporter (EAAT) substrate d-aspartate stimulates astrocytes to rap

127 nsporter, excitatory amino acid transporter (EAAT)-1, and the glutamate receptor subunit N-methyl-D-a

128 Excitatory amino acid transporter (EAAT)-2 is one of the major glutamate transporters prima

129 n and activity of the glutamate transporter (EAAT(2)) on glial cells, blocks methamphetamine-triggere

130 (GFAP, high affinity glutamate transporter (EAAT-2), apo-J (Clusterin), and peroxiredoxin-6) are sel

131 sporters (excitatory amino acid transporter (EAATs)) are critical for normal excitatory signaling and

132 of the "excitatory amino acid transporter" (EAAT) family.

133 udes the excitatory amino acid transporters (EAATs) and the prokaryotic aspartate transporter GltPh.

134 Excitatory amino acid transporters (EAATs) are a class of glutamate transporters that termin

135 Excitatory amino acid transporters (EAATs) are abundantly expressed by astrocytes, rapidly r

136 Excitatory amino acid transporters (EAATs) are crucial for glutamate homeostasis in the mamm

137 Excitatory amino acid transporters (EAATs) are crucial in maintaining extracellular levels o

138 Excitatory amino acid transporters (EAATs) are essential for terminating glutamatergic synap

139 Excitatory amino acid transporters (EAATs) are responsible for extracellular glutamate uptak

140 system, excitatory amino acid transporters (EAATs) are responsible for the clearance of glutamate af

141 Excitatory amino acid transporters (EAATs) are the primary regulators of extracellular gluta

142 Excitatory amino-acid transporters (EAATs) bind and transport glutamate, limiting spillover

143 Excitatory amino acid transporters (EAATs) buffer and remove synaptically released L-glutama

144 Excitatory amino acid transporters (EAATs) control the glutamate concentration in the synapt

145 ation of excitatory amino acid transporters (EAATs) for transmitter removal.

146 Excitatory amino acid transporters (EAATs) function as both substrate transporters and ligan

147 blocking excitatory amino acid transporters (EAATs) generates beam-like responses in Crus II.

148 space by excitatory amino acid transporters (EAATs) has been postulated to contribute to signal termi

149 ction of excitatory amino acid transporters (EAATs) in glia and postsynaptic neurons.

150 and the excitatory amino acid transporters (EAATs) in Glu uptake and recycling mechanisms leading to

151 the CNS, excitatory amino acid transporters (EAATs) localized to neurons and glia terminate the actio

152 Excitatory amino acid transporters (EAATs) located on neurons and glia are responsible for l

153 g of how excitatory amino acid transporters (EAATs) mediate chloride permeation and substrate transpo

154 The excitatory amino acid transporters (EAATs) play essential roles in regulating the synaptic c

155 Excitatory amino acid transporters (EAATs) remove glutamate from synapses.

156 Excitatory amino acid transporters (EAATs) terminate glutamatergic synaptic transmission by

157 Excitatory amino acid transporters (EAATs) terminate signaling in the CNS by clearing releas

158 Excitatory amino acid transporters (EAATs) use sodium and potassium gradients to remove glut

159 ed to as excitatory amino acid transporters (EAATs), are membrane proteins that regulate glutamatergi

160 acterial excitatory amino acid transporters (EAATs), as well as the crystal structure of a related ar

161 t by the excitatory amino acid transporters (EAATs), involving the cotransport of a proton and three

162 related excitatory amino acid transporters (EAATs), suggesting that this leak anion conductance is h

163 ifically excitatory amino acid transporters (EAATs), whose normal expression and regulation in the th

164 eins--or excitatory amino acid transporters (EAATs)--toward a similar end has been a road much less t

165 trocytic excitatory amino acid transporters (EAATs).

166 d by the excitatory amino-acid transporters (EAATs).

167 nown as "excitatory amino acid transporters (EAATs)." Here we cloned and functionally characterized t

168 porters (excitatory amino acid transporters, EAAT) play an important role in maintaining extracellula

169 porters (excitatory amino acid transporters, EAATs) and the prokaryotic aspartate transporter GltPh.

170 o called excitatory amino acid transporters, EAATs) bind extracellular glutamate and transport it to

171 porters (excitatory amino acid transporters; EAATs) exist exclusively in abluminal membranes.

172 addition to sodium-driven glutamate uptake, EAATs also mediate a glutamate-activated chloride conduc