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1 r and to the glycine transporters (GlyT1 and GlyT2).
2 lycine transporter (GlyT) isoforms GlyT1 and GlyT2.
3 interaction between the wild-type and mutant GlyT2.
4 ins 5, 7, and 8, and extracellular loop 4 of GlyT2.
5 uctural alterations of the S512R mutation in GlyT2.
6  other paralog showing greater similarity to GlyT2.
7 and how these bioactive lipids interact with GlyT2.
8 s-311-Cys-320 in the second external loop of GlyT2.
9 ansporter VGluT2 and the glycine transporter GlyT2.
10 igh-affinity glycine transporters, GlyT1 and GlyT2.
11 ansporter VGluT2 and the glycine transporter GlyT2.
12 hile inhibitors of glycine transport through GlyT2 (4-benzyloxy-3,5-dimethoxy-N-[1-(dimethylaminocycl
13 ergic neurons, or for glycine transporter 2 (GLYT2), a marker for glycinergic neurons.
14 ntrolling local Na(+) increases derived from GlyT2 activity after neurotransmitter release.
15 us PMCA and NCX activities are necessary for GlyT2 activity and that this modulation depends on lipid
16 enous regulatory mechanism that can modulate GlyT2 activity based on a compartmentalized interaction
17                               Alterations in GlyT2 activity modify glycinergic neurotransmission and
18       The ouabain-mediated downregulation of GlyT2 also occurs in vivo in two different systems: zebr
19 oding the presynaptic glycine transporter 2 (GlyT2), also cause hyperekplexia.
20 ic preBotC neurons of glycine transporter 2 (Glyt2, also known as Slc6a5)-Cre mice.
21  for sodium in the absence of substrate than GlyT2 and a gating mechanism that locks Na[Formula: see
22 unohistochemistry combined with ISH for both GlyT2 and GAD-67 mRNAs showed that at least 63% of midli
23 of preBotC inhibitory neurons expressed both GlyT2 and GAD2 while a much smaller subpopulation also e
24 ycine inhibitors, however, are selective for GlyT2 and have been shown to provide analgesia in animal
25  insight into the mechanism of inhibition of GlyT2 and highlights how lipids can modulate the activit
26 tochemistry analyses the association between GlyT2 and NKA was confirmed.
27 We find that the plasma membrane transporter GlyT2 and the intracellular enzyme glutamate decarboxyla
28 acts with the raft-associated active pool of GlyT2, and low and high levels of the specific NKA ligan
29 encoding the presynaptic glycine transporter GlyT2 are a second major cause of human hyperekplexia, a
30       Indeed, mutations in the gene encoding GlyT2 are the main presynaptic cause of hyperekplexia in
31       Indeed, mutations in the gene encoding GlyT2 are the main presynaptic cause of hyperekplexia in
32 ith the hypothesis that vertebrate GlyT1 and GlyT2 are, respectively, derived from GlyT1- and GlyT2-l
33 nate presynaptic glycine transporter (SLC6A5/GlyT2) are well-established genes of effect in hyperekpl
34  a trend for higher expression of VGLUT1 and GLYT2 around motor neurons in Trained versus Untrained r
35                                         Like GlyT2, ATB[Formula: see text] behaves as a unidirectiona
36                     The map of the GAD67 and GLYT2 axonal distribution revealed a gradient that runs
37  small nucleus of the midbrain tegmentum was GLYT2(+) but GFP(-) .
38 e middle ear ossicles, caused a reduction in Glyt2, but not Glyt1 mRNA in the ipsilateral DCN and in
39 S512R mutant formed oligomers with wild-type GlyT2 causing its retention in the ER.
40                      In the spinal cord, GFP/GLYT2(+) cells were observed in the dorsal and ventral h
41                      A few groups of GFP(+) /GLYT2(-) cells were observed in the midbrain and forebra
42                                              GlyT2 cotransports 3Na+/Cl-/glycine generating large ris
43                                      Using a GlyT2(Cre) mouse line, we show a subtype of ipRGCs restr
44                     We took advantage of the GlyT2-Cre mouse line (both male and female) to target ex
45 -mediated transfection of the flexed gene in GlyT2-Cre transgenic mice, evoked fast IPSCs in principa
46  rationalizing its phylogenetic proximity to GlyT2 despite their extreme divergence in specificity.
47                      The loss of presynaptic GlyT2 drastically impairs the refilling of glycinergic s
48 edullary slices from neonatal Dbx1(tdTomato);GlyT2(EGFP) and Dbx1(tdTomato);GAD1(EGFP) double reporte
49 ase [GAD]67-eGFP, and glycine transporter 2 (GlyT2)-eGFP, respectively).
50  excitability and morphology of glycinergic (GlyT2 expressing) ventral lumbar interneurons from SOD1G
51 c neurons, the neuronal glycine transporter (GLYT2) for glycinergic neurons, and glutamic acid decarb
52 c neurons, the neuronal glycine transporter (GLYT2) for glycinergic neurons, and glutamic acid decarb
53 Overexpression of calnexin rescued wild-type GlyT2 from the dominant negative effect of the mutant, i
54 ough the most common mechanism of disrupting GlyT2 function is protein truncation, new pathogenic mec
55                                              GlyT2 function is strictly coupled to the sodium electro
56 r mice expressing either tdTomato or EGFP in GlyT2(+), GAD1(+), or GAD2(+) neurons.
57                             We conclude that GlyT2(+)/GAD2(+) neurons modulate breathing rhythm by de
58 al terminals in the tissue, and the ratio of GLYT2/GAD67 in each pixel was calculated.
59 ic Na(+)/Cl(-)-dependent glycine transporter GlyT2 gene (SLC6A5) are rapidly emerging as a second maj
60 frameshift, and splice site mutations in the GlyT2 gene as the second major cause of startle disease.
61 eurons expressing the glycine transporter 2 (GlyT2) gene coexpress enhanced green fluorescent protein
62 , and a portion of these cells showed double GLYT2/GFP labeling.
63                                 We used a Tg(glyt2:gfp) transgenic zebrafish expressing the green flu
64  the human SLC6A5 gene encoding the neuronal GlyT2 glycine transporter are responsible for the presyn
65 type Cav3 channels; and 4) inhibition of the GLYT2 glycine transporter.
66 plex is found in lipid raft subdomains where GlyT2 has been previously found to be fully active.
67 late the endocytosis and total expression of GlyT2 in neurons.
68 ometry to identify proteins interacting with GlyT2 in the CNS.
69 inant negative effect that retains wild-type GlyT2 in the endoplasmic reticulum (ER), preventing surf
70                           Cells positive for GLYT2 include the commissural CoLAs as well as some of t
71  key role of the lipid tail interactions for GlyT2 inhibition.
72 l glycine uptake to 80% whereas the specific GlyT2 inhibitor Org 25543 had no effect.
73 e side effects of the very slowly reversible GlyT2 inhibitor, ORG25543 (2).
74 ns, to produce nanomolar affinity, selective GlyT2 inhibitors.
75 mal side effects, but are comparatively weak GlyT2 inhibitors.
76                                              GlyT2 interneurons were analysed according to their loca
77                                              GlyT2 interneurons were then divided into three subgroup
78                                              GlyT2 is the main supplier of glycine for vesicle refill
79 wo different glycine transporters, Glyt1 and Glyt2, is influenced by neuronal activity.
80                                  Cytoplasmic GlyT2 labelling was observed in a subset of Kv3.3-positi
81 of MNTB, and elevated glycine transporter 2 (GLYT2) levels.
82 2 are, respectively, derived from GlyT1- and GlyT2-like genes in invertebrate deuterostomes.
83  proteins constitute an outgroup to both the GlyT2-like proteins and to vertebrate GlyT1 sequences.
84                       In phylogenetic trees, GlyT2-like sequences from invertebrate deuterostomes for
85 A5 mutations result in defective subcellular GlyT2 localization, decreased glycine uptake or both, wi
86 itors LY 294002 and wortmannin on GlyT1- and GlyT2-mediated glycine uptake were investigated.
87                                              GlyT2 mediates synaptic glycine recycling, which constit
88  the glycine transporters 1 and 2 (GlyT1 and GlyT2)--members of the solute carrier family 6 (SLC6).
89            All BOTZ cells examined contained GLYT2 mRNA (n = 10), whereas none had detectable levels
90                   The duration of changes in Glyt2 mRNA evoked by unilateral labyrinthectomy, measure
91 ent activity, evoking localized increases in Glyt2 mRNA in clusters of neurons in the DCN.
92                                              GlyT2 mRNA was commonly found in the pre-BotC region but
93                                    Glyt1 and Glyt2 mRNA were measured by using hybridization histoche
94                        glyt1 and the related glyt2 mRNAs are expressed in the hindbrain and spinal co
95 sequencing of SLC6A5 revealed a new dominant GlyT2 mutation: pY705C (c.2114A-->G) in transmembrane do
96                     Although the majority of GlyT2 mutations detected so far are recessive, a dominan
97 d on a compartmentalized interaction between GlyT2, neuronal plasma membrane Ca(2+)-ATPase (PMCA) iso
98                                          Few GlyT2 neurons were activated.
99                Stimulation of 4 or 8 preBotC GlyT2(+) neurons during endogenous rhythm prolonged the
100                       Most of the GFP(+) and GLYT2(+) neurons were observed in the rhombencephalon an
101 where GABAergic (GAD1/2(+)) and glycinergic (GlyT2(+)) neurons are functionally and anatomically inte
102                     Pharmacological block of GlyT2 or glutamate decarboxylase led to rapid and comple
103 ing site on the human glycine transporter 2 (GlyT2 or SLC6A5).
104             The neuronal glycine transporter GlyT2 plays a fundamental role in the glycinergic neurot
105                                         This GlyT2.PMCA2,3.NCX1 complex is found in lipid raft subdom
106         Besides, we propose a model in which GlyT2.PMCA2-3.NCX complex would help Na(+)/K(+)-ATPase i
107                        In the hindbrain, GFP/GLYT2(+) populations were observed in the medial octavol
108                Reductions in the activity of GlyT2-positive cells produced mild increases in neural a
109 al domain, dual in situ staining showed that GLYT2-positive cells were intermingled with VGLUT2 cells
110                  The CiA cells were the only GLYT2-positive cells with an ipsilateral axon.
111 ore and after chemogenetic downregulation of GlyT2-positive interneurons in male and female mice.
112  results suggest that inhibition mediated by GlyT2-positive interneurons primarily governs the tempor
113         Here, we examine the contribution of GlyT2-positive interneurons to network dynamics in Crus
114                                              GlyT2-positive interneurons, Golgi and Lugaro cells, res
115 also performed in situ hybridization using a GLYT2 probe and glycine immunohistochemistry.
116  under control of the glycine transporter 2 (GLYT2) regulatory sequences to study for the first time
117 cing revealed three conspicuous pairs of GFP/GLYT2(+) reticular neurons projecting to the spinal cord
118 itors that target the glycine transporter 2, GlyT2, show promise as analgesics, but may be limited by
119 s that inhibit the human glycine transporter GlyT2 (SLC6A5) and provide analgesia in animal models of
120 he SLC6 family along with GlyT1 (SLC6A9) and GlyT2 (SLC6A5), two glycine-specific transporters couple
121 ic Na(+)/Cl(-)-dependent glycine transporter GlyT2 (SLC6A5).
122                                              GlyT2 subsequently diverged significantly from its inver
123 s at embryonic stages were also positive for GLYT2, suggesting that the cells might use both GABA and
124 minal by the neuronal glycine transporter 2 (GlyT2) to maintain quantal glycine content in synaptic v
125 ive, a dominant negative mutant that affects GlyT2 trafficking does exist.
126 , but had little or no activity at the human GlyT2 transporter, at other binding sites for glycine, o
127 dorsomedially in the ICC and relatively more GLYT2 ventrolaterally.
128                                              GLYT2 was seen only in the central nucleus of the IC (IC
129 ine transporters GlyT1A, GlyT1B, GlyT1C, and GlyT2 were stably expressed in QT6 cells.
130 form a monophyletic subclade with vertebrate GlyT2, while invertebrate GlyT1-like proteins constitute

 
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