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 was not associated with a faster decrease in SOFA s

4 EAAT was not independently associated with this outcome

5 EAAT-2 expression was inversely correlated with tumor gr

6 EAATs achieve million-fold transmitter gradients by symp

7 EAATs also mediate a thermodynamically uncoupled substra

8 EAATs are also chloride (Cl-) channels, but the physiolo

9 EAATs are glutamate transporters and anion-selective ion

10 EAATs are not only secondary active glutamate transporte

11 EAATs are trimeric proteins and are thought to comprise

12 EAATs reside on rod bipolar cell axon terminals where GA

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

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

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

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

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

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

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

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

21 system to characterize EAAT ligands for all EAAT subtypes.

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

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

24 mediated independently by each subunit of an EAAT multimer.

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

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

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

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

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

30 The relationship between EAAT and day 28 all-cause mortality (primary endpoint) w

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

32 ansport and anion channel properties of both EAAT isoforms.

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

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

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

36 llular glutamate and its local regulation by EAATs.

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

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

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

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

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

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

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

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

45 e responsible for the observed effect during EAAT suppression.

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

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

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

49 H9c2 expresses EAATs but lacks endogenous NCX1 expression.

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

51 Among five EAATs, EAAT3 is the only isoform that can efficiently tr

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

53 However, a prognostic benefit from EAAT cannot be ruled out due to lack of statistical powe

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

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

56 carriers, predominantly involving the glial EAAT 2 transporter.

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

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

59 Excess glutamate release and alteration in EAAT expression are associated with several CNS disorder

60 e affinity for the transported amino acid in EAATs.

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

62 s and is augmented by coupling to protons in EAATs.

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

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

65 ptosomal uptake with those of the individual EAAT clones.

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

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

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

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

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

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

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

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

74 This series also provides nonselective EAAT PAMs, EAAT inhibitors, and inactive compounds that

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

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

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

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

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

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

81 pneumonia types, causative GNB, features of EAAT, and the occurrence of septic shock at pneumonia di

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

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

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

85 y be useful for elucidating the mechanism of EAAT allosteric modulation.

86 studies have investigated the regulation of EAAT expression.

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

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

89 ntal data on substrate binding properties of EAATs.

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

91 series also provides nonselective EAAT PAMs, EAAT inhibitors, and inactive compounds that may be usef

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

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

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

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

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

97 embrane-reconstituted Glt(Ph), a prokaryotic EAAT homologue, with millisecond temporal resolution.

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

99 804 included patients, 495 (61.6%) received EAAT (single-drug, 25.4%; combination, 36.2%).

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

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

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

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

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

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

106 mphibian retina an excellent system to study EAAT function.

107 In this study, EAAT was not associated with a reduced day 28 mortality,

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

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

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

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

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

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

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

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

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

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

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

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

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

121 f anion channel gating processes outside the EAAT uptake cycle.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 hysiological role of Cl- conductance through EAATs is poorly understood.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Excitatory amino acid transporters (EAATs) are essential CNS proteins that regulate glutamat

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

157 Excitatory amino acid transporters (EAATs) are important in many physiological processes and

158 Excitatory amino acid transporters (EAATs) are prototypical dual function proteins that func

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 Excitatory amino acid transporters (EAATs) regulate extracellular glutamate by transporting

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

177 Excitatory amino acid transporters (EAATs) represent a protein family that is an emerging dr

178 Excitatory amino acid transporters (EAATs) reside on cell surfaces and uptake substrates, in

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

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

181 Excitatory amino acid transporters (EAATs) uptake glutamate into glial cells and neurons.

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

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

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

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

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

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

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

189 R6b) and Excitatory Amino Acid Transporters (EAATs).

190 known as excitatory amino acid transporters (EAATs).

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

192 trocytic excitatory amino acid transporters (EAATs).

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

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

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

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

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

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