ライフサイエンスコーパス: GlyT2

1 uctural alterations of the S512R mutation in GlyT2.

2 other paralog showing greater similarity to GlyT2.

3 lycine transporter (GlyT) isoforms GlyT1 and GlyT2.

4 interaction between the wild-type and mutant GlyT2.

5 s-311-Cys-320 in the second external loop of GlyT2.

6 ansporter VGluT2 and the glycine transporter GlyT2.

7 igh-affinity glycine transporters, GlyT1 and GlyT2.

8 ansporter VGluT2 and the glycine transporter GlyT2.

9 hile inhibitors of glycine transport through GlyT2 (4-benzyloxy-3,5-dimethoxy-N-[1-(dimethylaminocycl

10 ergic neurons, or for glycine transporter 2 (GLYT2), a marker for glycinergic neurons.

11 ntrolling local Na(+) increases derived from GlyT2 activity after neurotransmitter release.

12 us PMCA and NCX activities are necessary for GlyT2 activity and that this modulation depends on lipid

13 enous regulatory mechanism that can modulate GlyT2 activity based on a compartmentalized interaction

14 Alterations in GlyT2 activity modify glycinergic neurotransmission and

15 The ouabain-mediated downregulation of GlyT2 also occurs in vivo in two different systems: zebr

16 oding the presynaptic glycine transporter 2 (GlyT2), also cause hyperekplexia.

17 ic preBotC neurons of glycine transporter 2 (Glyt2, also known as Slc6a5)-Cre mice.

18 unohistochemistry combined with ISH for both GlyT2 and GAD-67 mRNAs showed that at least 63% of midli

19 tochemistry analyses the association between GlyT2 and NKA was confirmed.

20 We find that the plasma membrane transporter GlyT2 and the intracellular enzyme glutamate decarboxyla

21 acts with the raft-associated active pool of GlyT2, and low and high levels of the specific NKA ligan

22 encoding the presynaptic glycine transporter GlyT2 are a second major cause of human hyperekplexia, a

23 Indeed, mutations in the gene encoding GlyT2 are the main presynaptic cause of hyperekplexia in

24 Indeed, mutations in the gene encoding GlyT2 are the main presynaptic cause of hyperekplexia in

25 ith the hypothesis that vertebrate GlyT1 and GlyT2 are, respectively, derived from GlyT1- and GlyT2-l

26 nate presynaptic glycine transporter (SLC6A5/GlyT2) are well-established genes of effect in hyperekpl

27 a trend for higher expression of VGLUT1 and GLYT2 around motor neurons in Trained versus Untrained r

28 The map of the GAD67 and GLYT2 axonal distribution revealed a gradient that runs

29 small nucleus of the midbrain tegmentum was GLYT2(+) but GFP(-) .

30 e middle ear ossicles, caused a reduction in Glyt2, but not Glyt1 mRNA in the ipsilateral DCN and in

31 S512R mutant formed oligomers with wild-type GlyT2 causing its retention in the ER.

32 In the spinal cord, GFP/GLYT2(+) cells were observed in the dorsal and ventral h

33 A few groups of GFP(+) /GLYT2(-) cells were observed in the midbrain and forebra

34 GlyT2 cotransports 3Na+/Cl-/glycine generating large ris

35 We took advantage of the GlyT2-Cre mouse line (both male and female) to target ex

36 -mediated transfection of the flexed gene in GlyT2-Cre transgenic mice, evoked fast IPSCs in principa

37 The loss of presynaptic GlyT2 drastically impairs the refilling of glycinergic s

38 ase [GAD]67-eGFP, and glycine transporter 2 (GlyT2)-eGFP, respectively).

39 c neurons, the neuronal glycine transporter (GLYT2) for glycinergic neurons, and glutamic acid decarb

40 c neurons, the neuronal glycine transporter (GLYT2) for glycinergic neurons, and glutamic acid decarb

41 Overexpression of calnexin rescued wild-type GlyT2 from the dominant negative effect of the mutant, i

42 ough the most common mechanism of disrupting GlyT2 function is protein truncation, new pathogenic mec

43 GlyT2 function is strictly coupled to the sodium electro

44 al terminals in the tissue, and the ratio of GLYT2/GAD67 in each pixel was calculated.

45 ic Na(+)/Cl(-)-dependent glycine transporter GlyT2 gene (SLC6A5) are rapidly emerging as a second maj

46 frameshift, and splice site mutations in the GlyT2 gene as the second major cause of startle disease.

47 eurons expressing the glycine transporter 2 (GlyT2) gene coexpress enhanced green fluorescent protein

48 , and a portion of these cells showed double GLYT2/GFP labeling.

49 We used a Tg(glyt2:gfp) transgenic zebrafish expressing the green flu

50 the human SLC6A5 gene encoding the neuronal GlyT2 glycine transporter are responsible for the presyn

51 type Cav3 channels; and 4) inhibition of the GLYT2 glycine transporter.

52 plex is found in lipid raft subdomains where GlyT2 has been previously found to be fully active.

53 late the endocytosis and total expression of GlyT2 in neurons.

54 ometry to identify proteins interacting with GlyT2 in the CNS.

55 inant negative effect that retains wild-type GlyT2 in the endoplasmic reticulum (ER), preventing surf

56 Cells positive for GLYT2 include the commissural CoLAs as well as some of t

57 l glycine uptake to 80% whereas the specific GlyT2 inhibitor Org 25543 had no effect.

58 GlyT2 is the main supplier of glycine for vesicle refill

59 wo different glycine transporters, Glyt1 and Glyt2, is influenced by neuronal activity.

60 Cytoplasmic GlyT2 labelling was observed in a subset of Kv3.3-positi

61 2 are, respectively, derived from GlyT1- and GlyT2-like genes in invertebrate deuterostomes.

62 proteins constitute an outgroup to both the GlyT2-like proteins and to vertebrate GlyT1 sequences.

63 In phylogenetic trees, GlyT2-like sequences from invertebrate deuterostomes for

64 A5 mutations result in defective subcellular GlyT2 localization, decreased glycine uptake or both, wi

65 itors LY 294002 and wortmannin on GlyT1- and GlyT2-mediated glycine uptake were investigated.

66 GlyT2 mediates synaptic glycine recycling, which constit

67 the glycine transporters 1 and 2 (GlyT1 and GlyT2)--members of the solute carrier family 6 (SLC6).

68 All BOTZ cells examined contained GLYT2 mRNA (n = 10), whereas none had detectable levels

69 The duration of changes in Glyt2 mRNA evoked by unilateral labyrinthectomy, measure

70 ent activity, evoking localized increases in Glyt2 mRNA in clusters of neurons in the DCN.

71 GlyT2 mRNA was commonly found in the pre-BotC region but

72 Glyt1 and Glyt2 mRNA were measured by using hybridization histoche

73 glyt1 and the related glyt2 mRNAs are expressed in the hindbrain and spinal co

74 sequencing of SLC6A5 revealed a new dominant GlyT2 mutation: pY705C (c.2114A-->G) in transmembrane do

75 Although the majority of GlyT2 mutations detected so far are recessive, a dominan

76 d on a compartmentalized interaction between GlyT2, neuronal plasma membrane Ca(2+)-ATPase (PMCA) iso

77 Few GlyT2 neurons were activated.

78 Most of the GFP(+) and GLYT2(+) neurons were observed in the rhombencephalon an

79 Pharmacological block of GlyT2 or glutamate decarboxylase led to rapid and comple

80 The neuronal glycine transporter GlyT2 plays a fundamental role in the glycinergic neurot

81 This GlyT2.PMCA2,3.NCX1 complex is found in lipid raft subdom

82 Besides, we propose a model in which GlyT2.PMCA2-3.NCX complex would help Na(+)/K(+)-ATPase i

83 In the hindbrain, GFP/GLYT2(+) populations were observed in the medial octavol

84 al domain, dual in situ staining showed that GLYT2-positive cells were intermingled with VGLUT2 cells

85 The CiA cells were the only GLYT2-positive cells with an ipsilateral axon.

86 also performed in situ hybridization using a GLYT2 probe and glycine immunohistochemistry.

87 under control of the glycine transporter 2 (GLYT2) regulatory sequences to study for the first time

88 cing revealed three conspicuous pairs of GFP/GLYT2(+) reticular neurons projecting to the spinal cord

89 ic Na(+)/Cl(-)-dependent glycine transporter GlyT2 (SLC6A5).

90 GlyT2 subsequently diverged significantly from its inver

91 s at embryonic stages were also positive for GLYT2, suggesting that the cells might use both GABA and

92 minal by the neuronal glycine transporter 2 (GlyT2) to maintain quantal glycine content in synaptic v

93 ive, a dominant negative mutant that affects GlyT2 trafficking does exist.

94 , but had little or no activity at the human GlyT2 transporter, at other binding sites for glycine, o

95 dorsomedially in the ICC and relatively more GLYT2 ventrolaterally.

96 GLYT2 was seen only in the central nucleus of the IC (IC

97 ine transporters GlyT1A, GlyT1B, GlyT1C, and GlyT2 were stably expressed in QT6 cells.

98 form a monophyletic subclade with vertebrate GlyT2, while invertebrate GlyT1-like proteins constitute