PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34845374-6	2022	In vivo, we observed that combined 5-FU with Thiamet-G (O-GlcNAcase (OGA) inhibitor) treatment had a synergistic inhibitory effect on grade and tumor progression.	thiamet	45-52	O-GlcNAcase	Homo sapiens	56-67
18587388-3	2008	We describe the rational design and synthesis of such an inhibitor (thiamet-G, K(i) = 21 nM; 1) of human O-GlcNAcase.	thiamet	68-75	O-GlcNAcase	Homo sapiens	105-116
34845374-6	2022	In vivo, we observed that combined 5-FU with Thiamet-G (O-GlcNAcase (OGA) inhibitor) treatment had a synergistic inhibitory effect on grade and tumor progression.	thiamet	45-52	O-GlcNAcase	Homo sapiens	69-72
32365408-5	2021	Here we show that Thiamet-G, a highly selective pharmacological agent that inhibits the glycoside hydrolase O-GlcNAcase (OGA), blunts the cellular uptake of alpha-synuclein fibrils.	thiamet	18-25	O-GlcNAcase	Mus musculus	121-124
34741260-3	2022	Here, we found that injection of Thiamet G, an O-GlcNAcase (OGA) inhibitor, in the VTA and nucleus accumbens (NAc) of mice, facilitated neuronal O-GlcNAcylation and decreased the operant response to sucrose as well as the latency to fall in rotarod test.	thiamet	33-40	O-GlcNAcase	Mus musculus	60-63
35588599-6	2022	In acute AD model mice, 39 was more effective than Thiamet-G in inhibiting OGA activity attributable to its better blood-brain barrier permeability.	thiamet	51-58	O-GlcNAcase	Mus musculus	75-78
35588599-7	2022	In addition, 39 restored the cognitive function in mice and reduced amyloid-beta (Abeta) concentrations to a greater extent than Thiamet-G. Molecular docking studies demonstrated that 39 was well associated with OGA through H-bonds and hydrophobic interaction.	thiamet	129-136	O-GlcNAcase	Mus musculus	212-215
33600817-5	2021	In this study, using transient ischemic stroke models, we first demonstrated that neuron-specific overexpression of Xbp1s improved outcome, and pharmacologically boosting O-GlcNAcylation with thiamet-G reversed worse outcome observed in neuron-specific Xbp1 knockout mice.	thiamet	192-199	X-box binding protein 1	Mus musculus	116-120
34668190-7	2022	Alloxan and Thiamet G were used to reduce and increase global OGT glycosylation levels in C2C12 cells, respectively.	thiamet	12-19	O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase)	Mus musculus	62-65
34312767-5	2021	Intriguingly, REMSD-induced defects in L/M functions and FC-induced PKA/CREB activation were restored upon increasing O-GlcNAc cycling with glucosamine (GlcN) or Thiamet G. Furthermore, Thiamet G restored the REMSD-induced decrease in dendritic spine density.	thiamet	162-169	cAMP responsive element binding protein 1	Mus musculus	72-76
34312767-5	2021	Intriguingly, REMSD-induced defects in L/M functions and FC-induced PKA/CREB activation were restored upon increasing O-GlcNAc cycling with glucosamine (GlcN) or Thiamet G. Furthermore, Thiamet G restored the REMSD-induced decrease in dendritic spine density.	thiamet	186-193	cAMP responsive element binding protein 1	Mus musculus	72-76
32365408-5	2021	Here we show that Thiamet-G, a highly selective pharmacological agent that inhibits the glycoside hydrolase O-GlcNAcase (OGA), blunts the cellular uptake of alpha-synuclein fibrils.	thiamet	18-25	synuclein, alpha	Mus musculus	157-172
33023909-8	2020	Treatment with the O-GlcNAcase inhibitor Thiamet G or O-GlcNAc transferase (OGT) transfection, which increases O-GlcNAcylation, reduced SOCE activity, whereas treatment with the OGT inhibitor ST045849 or siOGT transfection, which decreases O-GlcNAcylation, also reduced SOCE activity.	thiamet	41-48	O-GlcNAcase	Homo sapiens	19-30
33023909-8	2020	Treatment with the O-GlcNAcase inhibitor Thiamet G or O-GlcNAc transferase (OGT) transfection, which increases O-GlcNAcylation, reduced SOCE activity, whereas treatment with the OGT inhibitor ST045849 or siOGT transfection, which decreases O-GlcNAcylation, also reduced SOCE activity.	thiamet	41-48	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	76-79
33023909-8	2020	Treatment with the O-GlcNAcase inhibitor Thiamet G or O-GlcNAc transferase (OGT) transfection, which increases O-GlcNAcylation, reduced SOCE activity, whereas treatment with the OGT inhibitor ST045849 or siOGT transfection, which decreases O-GlcNAcylation, also reduced SOCE activity.	thiamet	41-48	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	178-181
33086728-9	2020	Pharmacological elevation of protein O-GlcNAcylation using Thiamet G (TMG) or OGA siRNA increased Ang-2 levels.	thiamet	59-66	angiopoietin 2	Homo sapiens	98-103
30625365-6	2019	Inhibiting OGA with Thiamet-G elevated protein O-GlcNAcylation, and decreased both seizure duration and epileptic spike events, suggesting that OGA may be a therapeutic target for seizure control.	thiamet	20-27	O-GlcNAcase	Homo sapiens	11-14
31080560-4	2019	Hyper-O-GlcNAcylation (via 1 muM Thiamet-G/ThmG or 25 mM Glucose) enhanced the expression of EMT-associated genes (WNT5B and FOXC2), and protein expression of the EMT adhesion molecule, N-Cadherin.	thiamet	33-40	Wnt family member 5B	Homo sapiens	115-120
31080560-4	2019	Hyper-O-GlcNAcylation (via 1 muM Thiamet-G/ThmG or 25 mM Glucose) enhanced the expression of EMT-associated genes (WNT5B and FOXC2), and protein expression of the EMT adhesion molecule, N-Cadherin.	thiamet	33-40	forkhead box C2	Homo sapiens	125-130
31080560-4	2019	Hyper-O-GlcNAcylation (via 1 muM Thiamet-G/ThmG or 25 mM Glucose) enhanced the expression of EMT-associated genes (WNT5B and FOXC2), and protein expression of the EMT adhesion molecule, N-Cadherin.	thiamet	33-40	cadherin 2	Homo sapiens	186-196
31827688-3	2019	Here, we report that increased O-GlcNAcylation by the suppression of OGA activity using thiamet-G and OGA siRNA did not affect autophagy, whereas decreased O-GlcNAcylation caused by OGT inhibition by alloxan and OGT siRNA increased autophagy.	thiamet	88-95	O-GlcNAcase	Mus musculus	69-72
31092134-2	2019	Thiamet-G (O-GlcNAcase inhibitor) could upregulate protein O-GlcNAcylation level to improve dyskinesia in models of neurodegenerative diseases without any obvious detrimental side-effects.	thiamet	0-7	O-GlcNAcase	Rattus norvegicus	11-22
30625365-6	2019	Inhibiting OGA with Thiamet-G elevated protein O-GlcNAcylation, and decreased both seizure duration and epileptic spike events, suggesting that OGA may be a therapeutic target for seizure control.	thiamet	20-27	O-GlcNAcase	Homo sapiens	144-147
26728070-8	2016	Furthermore, inhibition of OGA activity by Thiamet G induced atrophy marker expression.	thiamet	43-50	O-GlcNAcase	Mus musculus	27-30
30221662-5	2018	Subsequently, the selective O-GlcNAcase inhibitor, thiamet G, increased the level of O-GlcNAc modification, which further disrupted autophagic flux; deteriorated cardiac diastolic function, as indicated by an increased left ventricular filling peak velocity/atrial contraction flow peak velocity ratio shown by echocardiography; and exacerbated myocardial abnormalities, as characterized by cardiomyocyte disorganization and fat and interstitial fibrosis accumulation.	thiamet	51-58	O-GlcNAcase	Rattus norvegicus	28-39
30086259-7	2018	In addition, the biological behaviors including proliferation and migration of PC-3 cells are also studied when OGA inhibitor Thiamet G is applied to elevate the total O-GlcNAcylation level.	thiamet	126-133	O-GlcNAcase	Homo sapiens	112-115
29196265-5	2018	Given that FOXM1 expression was reported to be elevated in gastric cancer, we examined the effect of high glucose or an inhibitor of O-GlcNAc hydrolase, Thiamet G (TMG), on FOXM1 protein expression in a human gastric cancer cell line, MKN45 cells, and confirmed that FOXM1 protein level and the cell proliferation were upregulated.	thiamet	153-160	forkhead box M1	Homo sapiens	173-178
29196265-5	2018	Given that FOXM1 expression was reported to be elevated in gastric cancer, we examined the effect of high glucose or an inhibitor of O-GlcNAc hydrolase, Thiamet G (TMG), on FOXM1 protein expression in a human gastric cancer cell line, MKN45 cells, and confirmed that FOXM1 protein level and the cell proliferation were upregulated.	thiamet	153-160	forkhead box M1	Homo sapiens	173-178
29435130-5	2018	Additionally, treatment with Thiamet G, O-GlcNAcase OGA inhibitor, increased expression of O-GlcNAcylation and sCLU, and high glucose increased levels of LXRs, SREBP-1 and sCLU in HeLa cells.	thiamet	29-36	sterol regulatory element binding transcription factor 1	Homo sapiens	160-167
28681591-6	2017	Thiamet G treatment increased O-GlcNAcylated p65, which subsequently enhanced CXCR4 expression levels.	thiamet	0-7	RELA proto-oncogene, NF-kB subunit	Homo sapiens	45-48
28681591-6	2017	Thiamet G treatment increased O-GlcNAcylated p65, which subsequently enhanced CXCR4 expression levels.	thiamet	0-7	C-X-C motif chemokine receptor 4	Homo sapiens	78-83
28392398-5	2017	Furthermore, both of PUGNAc and Thiamet-G treatment up-regulated the expression levels of alpha-1,4-galactosyltransferase/Gb3Cer synthase gene which encodes a key enzyme in Gb4Cer synthesis.	thiamet	32-39	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	90-121
28392398-5	2017	Furthermore, both of PUGNAc and Thiamet-G treatment up-regulated the expression levels of alpha-1,4-galactosyltransferase/Gb3Cer synthase gene which encodes a key enzyme in Gb4Cer synthesis.	thiamet	32-39	beta-1,3-N-acetylgalactosaminyltransferase 1 (globoside blood group)	Homo sapiens	173-179
28259907-4	2017	To investigate the effect of O-GlcNAcylation on ovarian cancer phenotypes, global O-GlcNAc levels were decreased by OGT silencing through RNA interference and increased by inhibiting OGA activity with Thiamet-G. Transwell assay results demonstrated that OGT silencing inhibited the migration and invasion of SKOV3 and 59M ovarian cells in vitro, while Thiamet-G treatment promoted migration and invasion.	thiamet	201-208	O-GlcNAcase	Homo sapiens	183-186
28259907-5	2017	Furthermore, a pull-down assay and western blot analysis demonstrated that Thiamet-G treatment enhanced RhoA activity and the phosphorylation of the Rho-associated protein kinase (ROCK) substrate, myosin light chain (MLC), while OGT silencing attenuated RhoA activity and MLC phosphorylation.	thiamet	75-82	ras homolog family member A	Homo sapiens	104-108
28259907-5	2017	Furthermore, a pull-down assay and western blot analysis demonstrated that Thiamet-G treatment enhanced RhoA activity and the phosphorylation of the Rho-associated protein kinase (ROCK) substrate, myosin light chain (MLC), while OGT silencing attenuated RhoA activity and MLC phosphorylation.	thiamet	75-82	modulator of VRAC current 1	Homo sapiens	197-215
28259907-5	2017	Furthermore, a pull-down assay and western blot analysis demonstrated that Thiamet-G treatment enhanced RhoA activity and the phosphorylation of the Rho-associated protein kinase (ROCK) substrate, myosin light chain (MLC), while OGT silencing attenuated RhoA activity and MLC phosphorylation.	thiamet	75-82	modulator of VRAC current 1	Homo sapiens	217-220
28259907-5	2017	Furthermore, a pull-down assay and western blot analysis demonstrated that Thiamet-G treatment enhanced RhoA activity and the phosphorylation of the Rho-associated protein kinase (ROCK) substrate, myosin light chain (MLC), while OGT silencing attenuated RhoA activity and MLC phosphorylation.	thiamet	75-82	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	229-232
28259907-5	2017	Furthermore, a pull-down assay and western blot analysis demonstrated that Thiamet-G treatment enhanced RhoA activity and the phosphorylation of the Rho-associated protein kinase (ROCK) substrate, myosin light chain (MLC), while OGT silencing attenuated RhoA activity and MLC phosphorylation.	thiamet	75-82	ras homolog family member A	Homo sapiens	254-258
28259907-5	2017	Furthermore, a pull-down assay and western blot analysis demonstrated that Thiamet-G treatment enhanced RhoA activity and the phosphorylation of the Rho-associated protein kinase (ROCK) substrate, myosin light chain (MLC), while OGT silencing attenuated RhoA activity and MLC phosphorylation.	thiamet	75-82	modulator of VRAC current 1	Homo sapiens	272-275
28259907-6	2017	In addition, RhoA silencing via RNA interference and inhibition of ROCK activity with Y-27632 prevented Thiamet-G-induced increases in cell migration and invasion.	thiamet	104-111	ras homolog family member A	Homo sapiens	13-17
30344511-3	2018	We aim to characterize interplay between phosphorylation and O-GlcNAcylation for desmin in primary cultures of cardiomyocyte by specific O-GlcNAcase (OGA) inhibition with thiamet G and silencing O-GlcNAc transferase (OGT) and, in perfused heart perfused with thiamet G in sham- and HF-rats.	thiamet	171-178	desmin	Rattus norvegicus	81-87
30344511-3	2018	We aim to characterize interplay between phosphorylation and O-GlcNAcylation for desmin in primary cultures of cardiomyocyte by specific O-GlcNAcase (OGA) inhibition with thiamet G and silencing O-GlcNAc transferase (OGT) and, in perfused heart perfused with thiamet G in sham- and HF-rats.	thiamet	171-178	O-GlcNAcase	Rattus norvegicus	150-153
30344511-3	2018	We aim to characterize interplay between phosphorylation and O-GlcNAcylation for desmin in primary cultures of cardiomyocyte by specific O-GlcNAcase (OGA) inhibition with thiamet G and silencing O-GlcNAc transferase (OGT) and, in perfused heart perfused with thiamet G in sham- and HF-rats.	thiamet	259-266	desmin	Rattus norvegicus	81-87
30075176-9	2018	KEY FINDINGS: High levels of O-GlcNAc, induced by Thiamet G incubation, increased vascular expression of JAK1, but decreased expression and activity of STAT3.	thiamet	50-57	Janus kinase 1	Mus musculus	105-109
30075176-10	2018	In addition, IL-10 levels were diminished in arteries treated with Thiamet G. Absence of IL-10, as well as augmented O-GlcNAcylation, increased vascular reactivity to constrictor stimuli, an effect that was abolished by ERK 1/2 inhibitor.	thiamet	67-74	interleukin 10	Mus musculus	13-18
30075176-10	2018	In addition, IL-10 levels were diminished in arteries treated with Thiamet G. Absence of IL-10, as well as augmented O-GlcNAcylation, increased vascular reactivity to constrictor stimuli, an effect that was abolished by ERK 1/2 inhibitor.	thiamet	67-74	interleukin 10	Mus musculus	89-94
30075176-10	2018	In addition, IL-10 levels were diminished in arteries treated with Thiamet G. Absence of IL-10, as well as augmented O-GlcNAcylation, increased vascular reactivity to constrictor stimuli, an effect that was abolished by ERK 1/2 inhibitor.	thiamet	67-74	mitogen-activated protein kinase 3	Mus musculus	220-227
29622561-5	2018	Thiamet G treatment did not increase A20 protein expression but did significantly enhance binding to TAX1BP1 (Tax1-binding protein 1), a key regulatory protein for A20 activity.	thiamet	0-7	Tax1 binding protein 1	Rattus norvegicus	101-108
29622561-5	2018	Thiamet G treatment did not increase A20 protein expression but did significantly enhance binding to TAX1BP1 (Tax1-binding protein 1), a key regulatory protein for A20 activity.	thiamet	0-7	Tax1 binding protein 1	Rattus norvegicus	110-132
29622561-6	2018	Adenovirus-mediated A20 overexpression further enhanced the effects of thiamet G on prevention of TNF-alpha (tumor necrosis factor-alpha)-induced IkappaB (inhibitor of kappaB) degradation, p65 phosphorylation, and increases in DNA-binding activity.	thiamet	71-78	tumor necrosis factor	Rattus norvegicus	98-107
29622561-6	2018	Adenovirus-mediated A20 overexpression further enhanced the effects of thiamet G on prevention of TNF-alpha (tumor necrosis factor-alpha)-induced IkappaB (inhibitor of kappaB) degradation, p65 phosphorylation, and increases in DNA-binding activity.	thiamet	71-78	tumor necrosis factor	Rattus norvegicus	109-136
29622561-6	2018	Adenovirus-mediated A20 overexpression further enhanced the effects of thiamet G on prevention of TNF-alpha (tumor necrosis factor-alpha)-induced IkappaB (inhibitor of kappaB) degradation, p65 phosphorylation, and increases in DNA-binding activity.	thiamet	71-78	synaptotagmin 1	Rattus norvegicus	189-192
29622561-7	2018	A20 overexpression enhanced the inhibitory effects of thiamet G on TNF-alpha-induced proinflammatory cytokine expression and vascular smooth muscle cell migration and proliferation, whereas silencing endogenous A20 by transfection of specific A20 shRNA significantly attenuated these inhibitory effects.	thiamet	54-61	tumor necrosis factor	Rattus norvegicus	67-76
29624602-4	2018	We found that both doxycycline and Thiamet G treatments starting at 2 months of age prevented the progression of hyperactivity, slowed brain atrophy, and reduced brain hyperphosphorylated tau.	thiamet	35-42	microtubule associated protein tau	Homo sapiens	188-191
28571750-6	2017	Using this microarray, we clearly observed OGA activity and also inhibition thereof by OGA inhibitor thiamet G. Interestingly, different levels of OGA activity were observed of lysates derived from different cancer cell lines.	thiamet	101-108	O-GlcNAcase	Homo sapiens	87-90
28571750-6	2017	Using this microarray, we clearly observed OGA activity and also inhibition thereof by OGA inhibitor thiamet G. Interestingly, different levels of OGA activity were observed of lysates derived from different cancer cell lines.	thiamet	101-108	O-GlcNAcase	Homo sapiens	87-90
28487326-0	2017	XBP1 (X-Box-Binding Protein-1)-Dependent O-GlcNAcylation Is Neuroprotective in Ischemic Stroke in Young Mice and Its Impairment in Aged Mice Is Rescued by Thiamet-G. BACKGROUND AND PURPOSE: Impaired protein homeostasis induced by endoplasmic reticulum dysfunction is a key feature of a variety of age-related brain diseases including stroke.	thiamet	155-162	X-box binding protein 1	Mus musculus	0-4
28487326-0	2017	XBP1 (X-Box-Binding Protein-1)-Dependent O-GlcNAcylation Is Neuroprotective in Ischemic Stroke in Young Mice and Its Impairment in Aged Mice Is Rescued by Thiamet-G. BACKGROUND AND PURPOSE: Impaired protein homeostasis induced by endoplasmic reticulum dysfunction is a key feature of a variety of age-related brain diseases including stroke.	thiamet	155-162	X-box binding protein 1	Mus musculus	6-29
28521765-9	2017	Sustained and substantial OGA inhibition via chronic treatment with Thiamet G leads to a significant reduction of aggregated tau and several phosphorylated tau species in the insoluble fraction of rTg4510 mouse brain and total tau in cerebrospinal fluid (CSF).	thiamet	68-75	O-GlcNAcase	Mus musculus	26-29
28521765-9	2017	Sustained and substantial OGA inhibition via chronic treatment with Thiamet G leads to a significant reduction of aggregated tau and several phosphorylated tau species in the insoluble fraction of rTg4510 mouse brain and total tau in cerebrospinal fluid (CSF).	thiamet	68-75	microtubule associated protein tau	Homo sapiens	125-128
28521765-9	2017	Sustained and substantial OGA inhibition via chronic treatment with Thiamet G leads to a significant reduction of aggregated tau and several phosphorylated tau species in the insoluble fraction of rTg4510 mouse brain and total tau in cerebrospinal fluid (CSF).	thiamet	68-75	microtubule associated protein tau	Homo sapiens	156-159
28521765-9	2017	Sustained and substantial OGA inhibition via chronic treatment with Thiamet G leads to a significant reduction of aggregated tau and several phosphorylated tau species in the insoluble fraction of rTg4510 mouse brain and total tau in cerebrospinal fluid (CSF).	thiamet	68-75	microtubule associated protein tau	Homo sapiens	156-159
28521765-10	2017	O-GlcNAcylated tau is elevated by Thiamet G treatment and is found primarily in the soluble 55 kD tau species, but not in the insoluble 64 kD tau species thought as the pathological entity.	thiamet	34-41	microtubule associated protein tau	Homo sapiens	15-18
26333304-11	2016	Although the cell invasion induced by Thiamet-G was reduced by Akt1 shRNA, it was still higher in comparison with that to the control (cells with Akt1 shRNA alone).	thiamet	38-45	AKT serine/threonine kinase 1	Homo sapiens	63-67
26333304-11	2016	Although the cell invasion induced by Thiamet-G was reduced by Akt1 shRNA, it was still higher in comparison with that to the control (cells with Akt1 shRNA alone).	thiamet	38-45	AKT serine/threonine kinase 1	Homo sapiens	146-150
26333304-12	2016	And Akt1 overexpression promoted Thiamet-G-induced cell invasion.	thiamet	33-40	AKT serine/threonine kinase 1	Homo sapiens	4-8
25937070-10	2015	This O-GlcNAcylation of eIF2alpha was reproduced in thiamet-G-injected mouse liver.	thiamet	52-59	eukaryotic translation initiation factor 2A	Mus musculus	24-33
27231347-4	2016	When WT beta-YAC bone marrow cells are treated with the OGA inhibitor Thiamet-G, the occupancy of OGT, OGA, and Mi2beta at the (A)gamma-globin promoter is increased.	thiamet	70-77	O-GlcNAcase	Homo sapiens	103-106
27231347-4	2016	When WT beta-YAC bone marrow cells are treated with the OGA inhibitor Thiamet-G, the occupancy of OGT, OGA, and Mi2beta at the (A)gamma-globin promoter is increased.	thiamet	70-77	chromodomain helicase DNA binding protein 4	Homo sapiens	112-119
27231347-4	2016	When WT beta-YAC bone marrow cells are treated with the OGA inhibitor Thiamet-G, the occupancy of OGT, OGA, and Mi2beta at the (A)gamma-globin promoter is increased.	thiamet	70-77	hemoglobin subunit gamma 1	Homo sapiens	128-142
26370562-10	2015	In CIA mice, ThiaMet-G significantly aggravated the severity of arthritis clinically and histologically, and it also increased CD4 + IFN-gamma + T cells and CD4 + IL-17+ T cells.	thiamet	13-20	CD4 antigen	Mus musculus	127-130
26370562-10	2015	In CIA mice, ThiaMet-G significantly aggravated the severity of arthritis clinically and histologically, and it also increased CD4 + IFN-gamma + T cells and CD4 + IL-17+ T cells.	thiamet	13-20	interferon gamma	Mus musculus	133-142
26370562-10	2015	In CIA mice, ThiaMet-G significantly aggravated the severity of arthritis clinically and histologically, and it also increased CD4 + IFN-gamma + T cells and CD4 + IL-17+ T cells.	thiamet	13-20	CD4 antigen	Mus musculus	157-160
26343633-7	2015	Moreover, the BZX2 induced tau aggregation was efficiently reduced by the treatment of Thiamet G, an inhibitor of O-GlcNAcase (OGA).	thiamet	87-94	microtubule associated protein tau	Homo sapiens	27-30
26343633-7	2015	Moreover, the BZX2 induced tau aggregation was efficiently reduced by the treatment of Thiamet G, an inhibitor of O-GlcNAcase (OGA).	thiamet	87-94	O-GlcNAcase	Homo sapiens	114-125
26343633-7	2015	Moreover, the BZX2 induced tau aggregation was efficiently reduced by the treatment of Thiamet G, an inhibitor of O-GlcNAcase (OGA).	thiamet	87-94	O-GlcNAcase	Homo sapiens	127-130
27231347-4	2016	When WT beta-YAC bone marrow cells are treated with the OGA inhibitor Thiamet-G, the occupancy of OGT, OGA, and Mi2beta at the (A)gamma-globin promoter is increased.	thiamet	70-77	O-GlcNAcase	Homo sapiens	56-59
27231347-4	2016	When WT beta-YAC bone marrow cells are treated with the OGA inhibitor Thiamet-G, the occupancy of OGT, OGA, and Mi2beta at the (A)gamma-globin promoter is increased.	thiamet	70-77	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	98-101
26635480-9	2015	The global O-GlcNAc level of intracellular proteins was up-regulated by OGA inhibitor Thiamet-G treatment or OGT over-expression.	thiamet	86-93	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	11-19
26635480-9	2015	The global O-GlcNAc level of intracellular proteins was up-regulated by OGA inhibitor Thiamet-G treatment or OGT over-expression.	thiamet	86-93	O-GlcNAcase	Homo sapiens	72-75
26635480-17	2015	Moreover, silence of Akt1 remarkably attenuated the increase of cell invasion induced by Thiamet-G treatment, but the invasion was still higher compared to Akt1-silenced only cells.	thiamet	89-96	AKT serine/threonine kinase 1	Homo sapiens	21-25
26635480-18	2015	In other words, Thiamet-G restored the invasion of Akt1-silenced thyroid cancer cells, but it was still lower relative to Thiamet-G-treated only cells.	thiamet	16-23	AKT serine/threonine kinase 1	Homo sapiens	51-55
26252736-6	2015	In addition, when global O-GlcNAcylation was enhanced by treating cells with Thiamet-G, PKM2 expression level was upregulated, but PKM2-specific activity was decreased.	thiamet	77-84	pyruvate kinase M1/2	Homo sapiens	88-92
26252736-6	2015	In addition, when global O-GlcNAcylation was enhanced by treating cells with Thiamet-G, PKM2 expression level was upregulated, but PKM2-specific activity was decreased.	thiamet	77-84	pyruvate kinase M1/2	Homo sapiens	131-135
26108188-6	2015	These signals were enhanced when the O-linked beta-N-acetylglucosaminidase (OGA) inhibitor Thiamet G was added to prevent the deglycosylation of the GlcNAc moiety(ies).	thiamet	91-98	O-GlcNAcase	Homo sapiens	37-74
26108188-6	2015	These signals were enhanced when the O-linked beta-N-acetylglucosaminidase (OGA) inhibitor Thiamet G was added to prevent the deglycosylation of the GlcNAc moiety(ies).	thiamet	91-98	O-GlcNAcase	Homo sapiens	76-79
24744147-4	2014	Administration of the O-GlcNAcase inhibitor thiamet G to mice also increased colonic expression of beta-catenin.	thiamet	44-51	catenin (cadherin associated protein), beta 1	Mus musculus	99-111
25268318-0	2014	Thiamet-G-mediated inhibition of O-GlcNAcase sensitizes human leukemia cells to microtubule-stabilizing agent paclitaxel.	thiamet	0-7	O-GlcNAcase	Homo sapiens	33-44
25268318-3	2014	Here, we show that the highly selective O-GlcNAcase (OGA) inhibitor thiamet-G significantly sensitized human leukemia cell lines to paclitaxel, with an approximate 10-fold leftward shift of IC50.	thiamet	68-75	O-GlcNAcase	Homo sapiens	40-51
25268318-3	2014	Here, we show that the highly selective O-GlcNAcase (OGA) inhibitor thiamet-G significantly sensitized human leukemia cell lines to paclitaxel, with an approximate 10-fold leftward shift of IC50.	thiamet	68-75	O-GlcNAcase	Homo sapiens	53-56
25268318-4	2014	Knockdown of OGA by siRNAs or inhibition of OGA by thiamet-G did not influence the cell viability.	thiamet	51-58	O-GlcNAcase	Homo sapiens	44-47
25268318-5	2014	Furthermore, we demonstrated that thiamet-G binds to OGA in competition with 4-methylumbelliferyl N-acetyl-beta-d-glucosaminide dehydrate, an analogue of O-GlcNAc UDP, thereby suppressing the activity of OGA.	thiamet	34-41	O-GlcNAcase	Homo sapiens	53-56
25268318-5	2014	Furthermore, we demonstrated that thiamet-G binds to OGA in competition with 4-methylumbelliferyl N-acetyl-beta-d-glucosaminide dehydrate, an analogue of O-GlcNAc UDP, thereby suppressing the activity of OGA.	thiamet	34-41	O-GlcNAcase	Homo sapiens	204-207
25268318-6	2014	Importantly, inhibition of OGA by thiamet-G decreased the phosphorylation of microtubule-associated protein Tau and caused alterations of microtubule network in cells.	thiamet	34-41	O-GlcNAcase	Homo sapiens	27-30
25268318-6	2014	Importantly, inhibition of OGA by thiamet-G decreased the phosphorylation of microtubule-associated protein Tau and caused alterations of microtubule network in cells.	thiamet	34-41	microtubule associated protein tau	Homo sapiens	77-111
22992728-5	2012	We demonstrated that acute activation of SOCE in neonatal cardiomyocytes resulted in STIM1 puncta formation, which was inhibited in a dose-dependent manner by increasing O-GlcNAc synthesis with glucosamine or inhibiting O-GlcNAcase with thiamet-G. Glucosamine and thiamet-G also inhibited SOCE and were associated with increased O-GlcNAc modification of STIM1.	thiamet	237-244	stromal interaction molecule 1	Homo sapiens	85-90
23946484-6	2013	However, gain of function cells treated with the O-GlcNAcase inhibitor Thiamet-G restored the assembly of the spindle and partially rescued histone phosphorylation.	thiamet	71-78	O-GlcNAcase	Homo sapiens	49-60
23524144-5	2013	Additionally, through altering the total O-GlcNAcylation level by OGT silencing or OGA inhibition, we found that the migration of OVCAR3 cells was dramatically enhanced by PUGNAc and Thiamet G treatment, and the migration ability of HO-8910PM cells was significantly inhibited by OGT silencing.	thiamet	183-190	O-GlcNAcase	Homo sapiens	83-86
24366041-7	2014	The increase in BRVEC O-GlcNAcylation induced by high glucose, as well as by thiamet G [an O-GlcNAcase (OGA) inhibitor] led to a reduction in occludin expression levels in vitro, which was prevented by treatment with OGT siRNA and alloxan.	thiamet	77-84	O-GlcNAcase	Mus musculus	91-102
24366041-7	2014	The increase in BRVEC O-GlcNAcylation induced by high glucose, as well as by thiamet G [an O-GlcNAcase (OGA) inhibitor] led to a reduction in occludin expression levels in vitro, which was prevented by treatment with OGT siRNA and alloxan.	thiamet	77-84	O-GlcNAcase	Mus musculus	104-107
24366041-7	2014	The increase in BRVEC O-GlcNAcylation induced by high glucose, as well as by thiamet G [an O-GlcNAcase (OGA) inhibitor] led to a reduction in occludin expression levels in vitro, which was prevented by treatment with OGT siRNA and alloxan.	thiamet	77-84	O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase)	Mus musculus	217-220
22992728-5	2012	We demonstrated that acute activation of SOCE in neonatal cardiomyocytes resulted in STIM1 puncta formation, which was inhibited in a dose-dependent manner by increasing O-GlcNAc synthesis with glucosamine or inhibiting O-GlcNAcase with thiamet-G. Glucosamine and thiamet-G also inhibited SOCE and were associated with increased O-GlcNAc modification of STIM1.	thiamet	264-271	stromal interaction molecule 1	Homo sapiens	85-90
22536363-8	2012	Investigation of the major tau kinases showed that acute delivery of a high dose of thiamet-G into the brain also led to a marked activation of glycogen synthase kinase-3beta (GSK-3beta), possibly as a consequence of down-regulation of its upstream regulating kinase, AKT.	thiamet	84-91	glycogen synthase kinase 3 beta	Mus musculus	144-174
22859309-6	2012	Thiamet-G also activated pERK, p-JNK, and p-p38 and the O-GlcNAcylation of Akt.	thiamet	0-7	thymoma viral proto-oncogene 1	Mus musculus	75-78
22777418-5	2012	d-GlcN and Thiamet-G pretreatment suppressed the TNF-alpha-induced hypocontractility and endothelial dysfunction.	thiamet	11-18	tumor necrosis factor	Homo sapiens	49-58
22777418-6	2012	Total protein O-GlcNAc levels were significantly higher in aortic segments treated with d-GlcN or Thiamet-G compared with controls.	thiamet	98-105	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	14-22
22536363-8	2012	Investigation of the major tau kinases showed that acute delivery of a high dose of thiamet-G into the brain also led to a marked activation of glycogen synthase kinase-3beta (GSK-3beta), possibly as a consequence of down-regulation of its upstream regulating kinase, AKT.	thiamet	84-91	glycogen synthase kinase 3 beta	Mus musculus	176-185
22536363-8	2012	Investigation of the major tau kinases showed that acute delivery of a high dose of thiamet-G into the brain also led to a marked activation of glycogen synthase kinase-3beta (GSK-3beta), possibly as a consequence of down-regulation of its upstream regulating kinase, AKT.	thiamet	84-91	thymoma viral proto-oncogene 1	Mus musculus	268-271
22536363-10	2012	These results suggest that acute high-dose thiamet-G injection can not only directly antagonize tau phosphorylation, but also stimulate GSK-3beta activity, with the downstream consequence being site-specific, bi-directional regulation of tau phosphorylation in the mammalian brain.	thiamet	43-50	glycogen synthase kinase 3 beta	Homo sapiens	136-145