ライフサイエンスコーパス: EAAT4

1 sporter excitatory amino acid transporter 4 (EAAT4).

2 and the excitatory amino acid transporter 4 (EAAT4).

3 II are aligned between parasagittal bands of EAAT4.

4 pe 5 (SCA5), correlating with alterations in EAAT4.

5 ndrite and soma, and both regions accumulate EAAT4.

6 utamate is approximately 1 in both EAAT3 and EAAT4.

7 in Purkinje cells expressing high levels of EAAT4.

8 and-gated channel properties associated with EAAT4.

9 ied in human brain: EAAT1, EAAT2, EAAT3, and EAAT4.

10 ization of WT beta-III spectrin and prevents EAAT4, a protein known to interact with beta-III spectri

11 s), nor did it block the current produced by EAAT4 and EAAC1 glutamate transporters in Purkinje cells

12 Studies of EAAT4 and EAAC1 indicate an extrasynaptic localization o

13 ized primarily in astrocytes, whereas EAAC1, EAAT4 and EAAT5 are neuronal.

14 2 and EAAT3 is demonstrated to extend to the EAAT4 and EAAT5 subtypes as well.

15 ss of beta-III spectrin function by studying EAAT4 and GLAST knockout mice as well as crosses of both

16 are most susceptible to the combined loss of EAAT4 and GLAST, with degeneration of proximal dendrites

17 We found marked differences in EAAT4 and GluRdelta2 by protein blot and cell fractionat

18 the intracellular carboxy-terminal domain of EAAT4 and modulate its glutamate transport activity.

19 EAAT1-5 in humans, and GLAST, GLT-1, EAAC1, EAAT4, and EAAT5 in rodents, respectively.

20 GLAST (EAAT1), GLT-1 (EAAT2), EAAC1 (EAAT3), EAAT4, and EAAT5.

21 are primarily astrocytic, whereas EAAC1 and EAAT4 are neuronal.

22 RAP41 and GTRAP48 (for glutamate transporter EAAT4 associated protein) that specifically interact wit

23 Purkinje cell-specific glutamate transporter EAAT4 at the plasma membrane.

24 but not mutant beta-III spectrin stabilizes EAAT4 at the plasma membrane.

25 shown to stabilize the glutamate transporter EAAT4 at the surface of the plasma membrane.

26 (CF)-PC synapses are absent in mice lacking EAAT4 but unchanged in mice lacking EAAC1, indicating th

27 I (aldolase C) and the glutamate transporter EAAT4 cluster in parasagittal zones that receive input f

28 zure disorder with significant reductions of EAAT4, EAAT1, GluRdelta, IP3R, and NCAM140.

29 four distinct cDNAs (EAAC1, GLT1, GLAST, and EAAT4) encoding Na+-dependent glutamate transporters hav

30 allows us to compare regions of high and low EAAT4-expressing PCs.

31 erns of PC subset loss, defined by zebrin II/EAAT4 expression domains, following neonatal viral infec

32 Expression of EAAT4 follows a parasagittal banding pattern that allows

33 at trafficking of both beta-III spectrin and EAAT4 from the Golgi is disrupted through failure of the

34 EAAT4 had a region-specific distribution; EAAT4 was main

35 wo glutamate transporters, EAAC1 (EAAT3) and EAAT4; however, their relative contribution to the uptak

36 Zebrin II and EAAT4 immunofluorescence analysis in PND21, PND28, PND42

37 quickly but that the actual cycling rate of EAAT4 in physiological conditions is slow; therefore, th

38 f arachidonic acid to oocytes expressing rat EAAT4 increased glutamate-induced currents to a similar

39 The excitatory amino acid transporter EAAT4 is expressed predominantly in Purkinje neurons in

40 ere the density of the glutamate transporter EAAT4 is high.

41 ted in EAAT4 knock-out mice, indicating that EAAT4 is not required for maintaining this aspect of CF

42 anged in mice lacking EAAC1, indicating that EAAT4 is preferentially involved in clearing glutamate f

43 T, superimposed on the earlier deficiency of EAAT4, is responsible for Purkinje cell loss and progres

44 ssue distribution of EAAC1, GLT1, GLAST, and EAAT4, it appears that there are additional glutamate tr

45 SCs between Z(+) and Z(-) zones persisted in EAAT4 knock-out mice, indicating that EAAT4 is not requi

46 In beta-III-/- mice EAAT4 levels are reduced from an early age.

47 EAAT4 levels increased in cerebellum with age.

48 risingly, a twofold difference in functional EAAT4 levels is sufficient to alter signaling to BG, alt

49 Our data demonstrate that EAAT4 loss, but not abnormal AMPA receptor composition,

50 e loss of GLAST appears to be independent of EAAT4 loss, highlighting that other aspects of Purkinje

51 ufficient to alter signaling to BG, although EAAT4 may only be responsible for removing a fraction of

52 ogous effects on GltPh simulations and EAAT2/EAAT4 measurements of single-channel currents and anion/

53 the Purkinje cell (PC)-specific transporter, EAAT4, near parallel fiber (PF) release sites controls t

54 us at PND42, with the loss of both zebrin II/EAAT4-negative and zebrin II/EAAT4-positive neurons.

55 by preferential apoptotic loss of zebrin II/EAAT4-negative PC subsets in the anterior vermis.

56 nt with early preferential loss of zebrin II/EAAT4-negative PCs in the vermis, the densities of micro

57 ronan receptor CD44 were higher in zebrin II/EAAT4-negative zones.

58 At PND84, zebrin II/EAAT4 patterning was abolished in the anterior cerebellu

59 essing the excitatory amino acid transporter EAAT4, physiologically relevant concentrations of arachi

60 both zebrin II/EAAT4-negative and zebrin II/EAAT4-positive neurons.

61 Using EAAT4 promoter-driven eGFP reporter mice together with p

62 Using EAAT4 reporter transgenic mice, we show that peripherall

63 ly to the excitatory amino acid transporter (EAAT4), the glutamate receptor delta, and other proteins

64 proteins that may be involved in regulating EAAT4--the glutamate transporter expressed predominately

65 ng and inactivation correlation on EAAT3 and EAAT4 to determine whether the glutamate-activated chlor

66 EAAT4 had a region-specific distribution; EAAT4 was mainly in cerebellum, localized to Purkinje ce

67 d a minor portion of total EAAT1, EAAT3, and EAAT4 were associated with lipid rafts.