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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
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
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
29 gating, suggesting that drugs which inhibit GlyT1 might have both cognitive enhancing and antipsycho
31 de with vertebrate GlyT2, while invertebrate GlyT1-like proteins constitute an outgroup to both the G
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
36 e transporter subtype 1 heterozygote mutant (GlyT1+/-), to determine how constitutive NMDAR hypo- and
43 sidering the clinical safety and efficacy of GlyT1 inhibitors in raising glycine levels in clinical t
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
48 cs previously shown to be weak inhibitors of GlyT1 likewise had similar potency against all three iso
52 inase inhibitors LY 294002 and wortmannin on GlyT1- and GlyT2-mediated glycine uptake were investigat
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
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
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
68 e-sensitive glycine receptors, and therefore GlyT1 antagonists also have potential for the treatment
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
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
79 xpressed principally in the lower CNS; while GlyT1 has activity in both the lower CNS and several reg
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