PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32712279-4 2020 GlyT2 is markedly expressed in brainstem, spinal cord and cerebellum, where it is responsible for glycine uptake into glycinergic and GABAergic terminals. Glycine 98-105 solute carrier family 6 member 5 Homo sapiens 0-5 32712301-2 2020 The extracellular glycine concentration is regulated synergistically by two high affinity, large capacity transporters GlyT1 and GlyT2. Glycine 18-25 solute carrier family 6 member 5 Homo sapiens 129-134 31223446-3 2019 Furthermore, the free energy perturbation calculations and molecular dynamics (MD) studies revealed the GlyT2 amino acid residues critical for the binding and selectivity of both Glycine and our Hit1 compound. Glycine 179-186 solute carrier family 6 member 5 Homo sapiens 104-109 31270129-4 2019 GlyT2 is the only SLC6 family member known to translocate glycine, Na+, and Cl- in a 1:3:1 stoichiometry. Glycine 58-65 solute carrier family 6 member 5 Homo sapiens 0-5 31604777-5 2019 SLC6A5 encodes the sodium- and chloride-dependent glycine transporter 2 (GlyT2), which recaptures glycine, a major inhibitory transmitter in the brainstem and spinal cord. Glycine 50-57 solute carrier family 6 member 5 Homo sapiens 0-6 31604777-5 2019 SLC6A5 encodes the sodium- and chloride-dependent glycine transporter 2 (GlyT2), which recaptures glycine, a major inhibitory transmitter in the brainstem and spinal cord. Glycine 50-57 solute carrier family 6 member 5 Homo sapiens 73-78 31621581-2 2019 We recently developed a series of bioactive lipids that inhibit the human glycine transporter GlyT2 (SLC6A5) and provide analgesia in animal models of pain. Glycine 74-81 solute carrier family 6 member 5 Homo sapiens 94-99 31621581-2 2019 We recently developed a series of bioactive lipids that inhibit the human glycine transporter GlyT2 (SLC6A5) and provide analgesia in animal models of pain. Glycine 74-81 solute carrier family 6 member 5 Homo sapiens 101-107 32714574-3 2017 The phenotype of a glycinergic neuron is determined by the expression of at least two proteins: GlyT2, a plasma membrane transporter of glycine, and VIAAT, a vesicular transporter shared by glycine and GABA. Glycine 19-26 solute carrier family 6 member 5 Homo sapiens 96-101 29859229-3 2019 One of the most frequent causes of hyperekplexia are mutations in the SLC6A5 gene, encoding the neuronal glycine transporter 2 (GlyT2), a key component of inhibitory glycinergic presynapses involved in synaptic glycine recycling though sodium and chloride-dependent co-transport. Glycine 105-112 solute carrier family 6 member 5 Homo sapiens 70-76 29859229-3 2019 One of the most frequent causes of hyperekplexia are mutations in the SLC6A5 gene, encoding the neuronal glycine transporter 2 (GlyT2), a key component of inhibitory glycinergic presynapses involved in synaptic glycine recycling though sodium and chloride-dependent co-transport. Glycine 105-112 solute carrier family 6 member 5 Homo sapiens 128-133 28734869-2 2017 The neuronal glycine transporter 2 (GlyT2) is involved in the recycling of synaptic glycine from the inhibitory synaptic cleft and its activity modulates intra and extracellular glycine concentrations. Glycine 13-20 solute carrier family 6 member 5 Homo sapiens 36-41 28734869-2 2017 The neuronal glycine transporter 2 (GlyT2) is involved in the recycling of synaptic glycine from the inhibitory synaptic cleft and its activity modulates intra and extracellular glycine concentrations. Glycine 84-91 solute carrier family 6 member 5 Homo sapiens 13-34 28734869-2 2017 The neuronal glycine transporter 2 (GlyT2) is involved in the recycling of synaptic glycine from the inhibitory synaptic cleft and its activity modulates intra and extracellular glycine concentrations. Glycine 84-91 solute carrier family 6 member 5 Homo sapiens 36-41 29086036-2 2018 Prominent examples include mutations in the transporters for dopamine (DAT, SLC6A3), for creatine (CT1, SLC6A8), and for glycine (GlyT2, SLC6A5), which result in infantile dystonia, mental retardation, and hyperekplexia, respectively. Glycine 121-128 solute carrier family 6 member 5 Homo sapiens 130-135 29086036-2 2018 Prominent examples include mutations in the transporters for dopamine (DAT, SLC6A3), for creatine (CT1, SLC6A8), and for glycine (GlyT2, SLC6A5), which result in infantile dystonia, mental retardation, and hyperekplexia, respectively. Glycine 121-128 solute carrier family 6 member 5 Homo sapiens 137-143 32714574-3 2017 The phenotype of a glycinergic neuron is determined by the expression of at least two proteins: GlyT2, a plasma membrane transporter of glycine, and VIAAT, a vesicular transporter shared by glycine and GABA. Glycine 136-143 solute carrier family 6 member 5 Homo sapiens 96-101 23994185-4 2013 The glycine transporter 2 (GlyT2) regulates the uptake of glycine into presynaptic boutons. Glycine 4-11 solute carrier family 6 member 5 Homo sapiens 27-32 24962068-4 2014 N-arachidonyl-glycine (NAGly) is an endogenous lipid that inhibits glycine transport by GlyT2 and also shows potential as an analgesic, which may be further exploited in drug development. Glycine 14-21 solute carrier family 6 member 5 Homo sapiens 88-93 25837937-7 2015 Therefore, GT-0198 is considered to exhibit its analgesic effect via the activation of a glycine receptor by glycine following presynaptic GlyT2 inhibition in the spinal cord. Glycine 89-96 solute carrier family 6 member 5 Homo sapiens 139-144 25480793-5 2015 GlyT2 mediates synaptic glycine recycling, which constitutes the main source of releasable transmitter at glycinergic synapses. Glycine 24-31 solute carrier family 6 member 5 Homo sapiens 0-5 25315779-2 2014 After synaptic vesicle fusion, glycine is recovered back to the presynaptic terminal by the neuronal glycine transporter 2 (GlyT2) to maintain quantal glycine content in synaptic vesicles. Glycine 31-38 solute carrier family 6 member 5 Homo sapiens 101-122 25315779-2 2014 After synaptic vesicle fusion, glycine is recovered back to the presynaptic terminal by the neuronal glycine transporter 2 (GlyT2) to maintain quantal glycine content in synaptic vesicles. Glycine 31-38 solute carrier family 6 member 5 Homo sapiens 124-129 25315779-2 2014 After synaptic vesicle fusion, glycine is recovered back to the presynaptic terminal by the neuronal glycine transporter 2 (GlyT2) to maintain quantal glycine content in synaptic vesicles. Glycine 101-108 solute carrier family 6 member 5 Homo sapiens 124-129 23650557-2 2013 Mutations in the human GlyT2 gene (SLC6A5) that cause deficient glycine transport or defective GlyT2 trafficking are the second most common cause of hyperekplexia or startle disease. Glycine 64-71 solute carrier family 6 member 5 Homo sapiens 23-28 23650557-1 2013 The neuronal transporter GlyT2 is a polytopic, 12-transmembrane domain, plasma membrane glycoprotein involved in the removal and recycling of synaptic glycine from inhibitory synapses. Glycine 151-158 solute carrier family 6 member 5 Homo sapiens 25-30 23650557-2 2013 Mutations in the human GlyT2 gene (SLC6A5) that cause deficient glycine transport or defective GlyT2 trafficking are the second most common cause of hyperekplexia or startle disease. Glycine 64-71 solute carrier family 6 member 5 Homo sapiens 35-41 22132725-3 2012 In contrast, neuronal GLYT2 supplies glycine to the presynaptic terminal with a 3:1:1 stoichiometry. Glycine 37-44 solute carrier family 6 member 5 Homo sapiens 22-27 16884688-3 2006 Here, we describe mutations within the neuronal glycine transporter 2 gene (GLYT2, or SLC6A5, ) of hyperekplexia patients, whose symptoms cannot be attributed to glycine receptor mutations. Glycine 48-55 solute carrier family 6 member 5 Homo sapiens 76-81 21910806-2 2011 The neuronal glycine transporter 2 (GLYT2) supplies the terminal with substrate to refill synaptic vesicles containing glycine. Glycine 13-20 solute carrier family 6 member 5 Homo sapiens 36-41 18266927-1 2008 The neuronal glycine transporter GLYT2 is a plasma membrane protein that removes the neurotransmitter glycine from the synaptic cleft, thereby aiding the pre-synaptic terminal reloading and the termination of the glycinergic signal. Glycine 13-20 solute carrier family 6 member 5 Homo sapiens 33-38 16884688-3 2006 Here, we describe mutations within the neuronal glycine transporter 2 gene (GLYT2, or SLC6A5, ) of hyperekplexia patients, whose symptoms cannot be attributed to glycine receptor mutations. Glycine 48-55 solute carrier family 6 member 5 Homo sapiens 86-92 15265500-1 2004 A series of benzoylpiperidine analogs related to 4a was prepared, and their ability to inhibit the uptake of [(14)C]-glycine in COS7 cells transfected with human glycine transporter type-2 (GlyT-2) was evaluated. Glycine 117-124 solute carrier family 6 member 5 Homo sapiens 162-188 16751771-7 2006 SLC6A5 mutations result in defective subcellular GlyT2 localization, decreased glycine uptake or both, with selected mutations affecting predicted glycine and Na+ binding sites. Glycine 79-86 solute carrier family 6 member 5 Homo sapiens 0-6 16751771-7 2006 SLC6A5 mutations result in defective subcellular GlyT2 localization, decreased glycine uptake or both, with selected mutations affecting predicted glycine and Na+ binding sites. Glycine 147-154 solute carrier family 6 member 5 Homo sapiens 0-6 15374578-5 2004 Typical antipsychotics haloperidol, thioridazine and chlorpromazine non-selectively inhibited [(14)C]glycine uptake mediated by GlyT1a and GlyT2 with potency of 9-21 microM. Glycine 101-108 solute carrier family 6 member 5 Homo sapiens 139-144 11278707-5 2001 We found that, under conditions that stimulate vesicular glycine release, GLYT2 is rapidly trafficked first toward the plasma membrane and then internalized. Glycine 57-64 solute carrier family 6 member 5 Homo sapiens 74-79 14675166-5 2004 Incubation of a GlyT2 N-terminal fusion protein with spinal cord extract in the presence of calcium followed by protein sequence analysis localized the major N-terminal cleavage site after methionine 156, with a second cleavage site being situated after glycine 164. Glycine 254-261 solute carrier family 6 member 5 Homo sapiens 16-21 33794243-3 2021 Mutations in the human SLC6A5 gene encoding the neuronal glycine transporter GlyT2 may disrupt the inhibitory glycinergic neurotransmission and cause a presynaptic form of the disease. Glycine 57-64 solute carrier family 6 member 5 Homo sapiens 23-29 33794243-3 2021 Mutations in the human SLC6A5 gene encoding the neuronal glycine transporter GlyT2 may disrupt the inhibitory glycinergic neurotransmission and cause a presynaptic form of the disease. Glycine 57-64 solute carrier family 6 member 5 Homo sapiens 77-82 33765249-0 2022 Calcium-Dependent Regulation of the Neuronal Glycine Transporter GlyT2 by M2 Muscarinic Acetylcholine Receptors. Glycine 45-52 solute carrier family 6 member 5 Homo sapiens 65-70 33765249-1 2022 The neuronal glycine transporter GlyT2 modulates inhibitory glycinergic neurotransmission and plays a key role in regulating nociceptive signal progression. Glycine 13-20 solute carrier family 6 member 5 Homo sapiens 33-38 34266921-4 2021 We present an example of stimulus induced hyperekplexia captured on video EEG in a 7-week-old girl with compound heterozygous variants in the presynaptic glycine transporter gene SLC6A5. Glycine 154-161 solute carrier family 6 member 5 Homo sapiens 179-185