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1                                              GlyT1 -/+ mice showed a more rapid acquisition of sensit
2                                              GlyT1 inhibitors ALX 5407 and sarcosine reduced total gl
3                                              GlyT1+/- mice also had elevated protein expression of NR
4 t administration of a glycine transporter 1 (GlyT1) inhibitor, or molecular GlyT1 knockdown, in the d
5 udy we tested several glycine transporter 1 (GlyT1) inhibitors including NFPS, SSR 504734, Lu AA21279
6 elective inhibitor of glycine transporter 1 (GlyT1), and characterized its activity using a quail fib
7 loride (Org 25935), a glycine transporter-1 (GlyT1) inhibitor, and placebo pretreatment on ketamine-i
8  by inhibition of the glycine-transporter-1 (GlyT1).
9  from the synapse via glycine transporter-1 (GlyT1).
10 rms of the human glycine transporter type 1 (GlyT1).
11 tic areas by the glycine transporter type 1 (GlyT1).
12      (2) Activation of glycine transporter 1(GlyT1) induced by VEGF led to an increase in intracellul
13  action of the glycine transporters 1 and 2 (GlyT1 and GlyT2)--members of the solute carrier family 6
14 nstrates for the first time in humans that a GlyT1 inhibitor reduces the effects induced by NMDA rece
15 matic remission or previous treatment with a GlyT1 inhibitor or any other investigational drug.
16                                          All GlyT1 inhibitors increased seizure thresholds dose-depen
17 ring inhibitors that might distinguish among GlyT1 isoforms.
18 ctive glycine-reuptake inhibitor mediated by GlyT1, offer an alternative approach.
19 ulation of dopaminergic neurotransmission by GlyT1 inhibition.
20 we generated mice in which the gene encoding GlyT1 was inactivated by homologous recombination throug
21 blocker, glycine and a substrate agonist for GlyT1, sarcosine, induced voltage-dependent inward curre
22  consistent with positive immunostaining for GlyT1 in Bergmann glia while inhibitors of glycine trans
23 T1 and GlyT2 are, respectively, derived from GlyT1- and GlyT2-like genes in invertebrate deuterostome
24 ermine whether these glia express functional GlyT1 that can mediate both glycine uptake and efflux.
25 t time that Bergmann glia express functional GlyT1 that can work in reverse at near-physiological ion
26 vealed no transcripts in newborn homozygous [GlyT1(-/-)] mice and a 50% reduction in heterozygous (HZ
27 ce and a 50% reduction in heterozygous (HZ) [GlyT1(+/-)] mice as compared with WT littermates.
28 at result in decreased (SR-/-) or increased (GlyT1-/+) NMDA receptor signaling.
29  gating, suggesting that drugs which inhibit GlyT1 might have both cognitive enhancing and antipsycho
30                               Interestingly, GlyT1, the glial glycine transporter, regulates the stre
31 de with vertebrate GlyT2, while invertebrate GlyT1-like proteins constitute an outgroup to both the G
32  and the glycine transporter (GlyT) isoforms GlyT1 and GlyT2.
33 ed PI3 kinase blocker LY 294002 may modulate GlyT1 function independent of PI3 kinase inhibition.
34 ransporter 1 (GlyT1) inhibitor, or molecular GlyT1 knockdown, in the dorsal vagal complex (DVC) suppr
35                                    Moreover, GlyT1+/- mice had elevated amounts of GluR1 and GluR2 in
36 e transporter subtype 1 heterozygote mutant (GlyT1+/-), to determine how constitutive NMDAR hypo- and
37 d glycine transporter 1 heterozygous mutant (GlyT1-/+).
38 ups have focused on the development of novel GlyT1 inhibitors.
39                          Kinetic analysis of GlyT1 revealed the Km value of 27+/-1.5 microM and Vmax
40                                  Blockade of GlyT1 also caused a profound increase in the baseline cu
41 ogenous screening assay for the detection of GlyT1 antagonists.
42                      Antisense knock-down of GlyT1 in wild-type embryos phenocopies sho, and injectio
43 sidering the clinical safety and efficacy of GlyT1 inhibitors in raising glycine levels in clinical t
44                  Thus, reduced expression of GlyT1 enhances hippocampal NMDAR function and memory ret
45 se data suggest that selective inhibition of GlyT1 can enhance NMDAR-sensitive activity in vivo and a
46 luation of the hypothesis that inhibition of GlyT1 may increase synaptic glycine and thereby potentia
47                                Inhibition of GlyT1 reduced the frequency of spontaneous network event
48 cs previously shown to be weak inhibitors of GlyT1 likewise had similar potency against all three iso
49 ther study of the antipsychotic potential of GlyT1 inhibitors.
50          To characterize further the role of GlyT1, we generated mice in which the gene encoding GlyT
51 g a mechanism of uncompetitive inhibition on GlyT1-mediated glycine uptake.
52 inase inhibitors LY 294002 and wortmannin on GlyT1- and GlyT2-mediated glycine uptake were investigat
53 ive doses (MEDs) in the MEST test than other GlyT1 inhibitors.
54                  IC(50) values for reference GlyT1 inhibitors ALX-5407 (Allelix), (S)-13h (Merck), an
55 mine the efficacy of bitopertin, a selective GlyT1-mediated glycine-reuptake inhibitor, as an adjunct
56 recent description of a potent and selective GlyT1 inhibitor (N-[3-(4'-fluorophenyl)-3-(4'-phenylphen
57                       The glial GlyT subtype GlyT1 is well located to activate NMDA receptors.
58 These findings provide proof of concept that GlyT1 inhibition in the brain improves glucose and energ
59 ivity in vivo and also support the idea that GlyT1 may represent a novel target for developing therap
60 al trials for schizophrenia, we propose that GlyT1 inhibitors have the potential to be repurposed as
61 ta from transgenic mouse models suggest that GlyT1 might also play a role in terminating the actions
62                                          The GlyT1 transport inhibitors sarcosine, ALX-5407, and Org-
63  294002, a PI3 kinase inhibitor, blocked the GlyT1-mediated glycine uptake with an IC50 value of 81+/
64 glycine uptake was completely blocked by the GlyT1 inhibitors ALX 5407 and sarcosine, suggesting that
65 ompletely inhibited glycine transport in the GlyT1 cells, with an IC(50) value of 3 nM, but had littl
66 f lOFC neurons and reduced expression of the GlyT1 transporter.
67 ecessary mediator in VEGF signalling via the GlyT1-glycine-mTOR-VDAC1 axis pathway.
68 e-sensitive glycine receptors, and therefore GlyT1 antagonists also have potential for the treatment
69      Inhibitors of glycine transport through GlyT1 (sarcosine and (N-[3-(4'-fluorophenyl)-3-(4'-pheny
70  and higher alignment scores with respect to GlyT1 and the other paralog showing greater similarity t
71 6a9 gene that encodes a glycine transporter (GlyT1) was identified as the cause of the sho phenotype.
72 tudies suggest that the glycine transporter, GlyT1, maintains subsaturating concentrations of glycine
73 ependent high-affinity glycine transporters, GlyT1 and GlyT2.
74  phenocopies sho, and injection of wild-type GlyT1 mRNA into mutants rescues them.
75 present data show that, akin to GABA uptake, GlyT1 exerts a powerful modulatory action on network eve
76 nsistent with the hypothesis that vertebrate GlyT1 and GlyT2 are, respectively, derived from GlyT1- a
77 th the GlyT2-like proteins and to vertebrate GlyT1 sequences.
78 nity glycine uptake occurs predominantly via GlyT1.
79 xpressed principally in the lower CNS; while GlyT1 has activity in both the lower CNS and several reg
80 ssibility that LY 294002 might interact with GlyT1.

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