PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32371316-5	2020	BrdU proliferation assays showed that treatment with GPR39 agonist TC-G 1008 (100 nM and 1 muM) increased cell proliferation.	GPR39-C3	67-76	G protein-coupled receptor 39	Homo sapiens	53-58
34645465-0	2021	Activation of GPR39 with TC-G 1008 attenuates neuroinflammation via SIRT1/PGC-1alpha/Nrf2 pathway post-neonatal hypoxic-ischemic injury in rats.	GPR39-C3	25-34	G protein-coupled receptor 39	Rattus norvegicus	14-19
34645465-0	2021	Activation of GPR39 with TC-G 1008 attenuates neuroinflammation via SIRT1/PGC-1alpha/Nrf2 pathway post-neonatal hypoxic-ischemic injury in rats.	GPR39-C3	25-34	sirtuin 1	Rattus norvegicus	68-73
34645465-0	2021	Activation of GPR39 with TC-G 1008 attenuates neuroinflammation via SIRT1/PGC-1alpha/Nrf2 pathway post-neonatal hypoxic-ischemic injury in rats.	GPR39-C3	25-34	PPARG coactivator 1 alpha	Rattus norvegicus	74-84
34645465-0	2021	Activation of GPR39 with TC-G 1008 attenuates neuroinflammation via SIRT1/PGC-1alpha/Nrf2 pathway post-neonatal hypoxic-ischemic injury in rats.	GPR39-C3	25-34	NFE2 like bZIP transcription factor 2	Rattus norvegicus	85-89
34645465-11	2021	Moreover, TC-G 1008 treatment significantly increased the expression of SIRT1, PGC-1alpha and Nrf2, but downregulated the expressions of IL-6, IL-1beta, and TNF-alpha.	GPR39-C3	10-19	sirtuin 1	Rattus norvegicus	72-77
34645465-11	2021	Moreover, TC-G 1008 treatment significantly increased the expression of SIRT1, PGC-1alpha and Nrf2, but downregulated the expressions of IL-6, IL-1beta, and TNF-alpha.	GPR39-C3	10-19	PPARG coactivator 1 alpha	Rattus norvegicus	79-89
34645465-11	2021	Moreover, TC-G 1008 treatment significantly increased the expression of SIRT1, PGC-1alpha and Nrf2, but downregulated the expressions of IL-6, IL-1beta, and TNF-alpha.	GPR39-C3	10-19	NFE2 like bZIP transcription factor 2	Rattus norvegicus	94-98
34645465-11	2021	Moreover, TC-G 1008 treatment significantly increased the expression of SIRT1, PGC-1alpha and Nrf2, but downregulated the expressions of IL-6, IL-1beta, and TNF-alpha.	GPR39-C3	10-19	interleukin 6	Rattus norvegicus	137-141
34645465-11	2021	Moreover, TC-G 1008 treatment significantly increased the expression of SIRT1, PGC-1alpha and Nrf2, but downregulated the expressions of IL-6, IL-1beta, and TNF-alpha.	GPR39-C3	10-19	interleukin 1 alpha	Rattus norvegicus	143-151
34645465-11	2021	Moreover, TC-G 1008 treatment significantly increased the expression of SIRT1, PGC-1alpha and Nrf2, but downregulated the expressions of IL-6, IL-1beta, and TNF-alpha.	GPR39-C3	10-19	tumor necrosis factor	Rattus norvegicus	157-166
34645465-13	2021	CONCLUSIONS: TC-G 1008 attenuated neuroinflammation in part via the SIRT1/PGC-1alpha/Nrf2 pathway in a neonatal rat model of HIE.	GPR39-C3	13-22	sirtuin 1	Rattus norvegicus	68-73
34645465-13	2021	CONCLUSIONS: TC-G 1008 attenuated neuroinflammation in part via the SIRT1/PGC-1alpha/Nrf2 pathway in a neonatal rat model of HIE.	GPR39-C3	13-22	PPARG coactivator 1 alpha	Rattus norvegicus	74-84
34645465-13	2021	CONCLUSIONS: TC-G 1008 attenuated neuroinflammation in part via the SIRT1/PGC-1alpha/Nrf2 pathway in a neonatal rat model of HIE.	GPR39-C3	13-22	NFE2 like bZIP transcription factor 2	Rattus norvegicus	85-89
32371316-6	2020	TC-G 1008 also enhanced ERK phosphorylation in time- and concentration-dependent manners.	GPR39-C3	0-9	mitogen-activated protein kinase 1	Homo sapiens	24-27
32371316-10	2020	Of particular importance, wortmannin, U0126, and FR180204 (ERK inhibitor) abrogated the effect of TC-G 1008-induced cell proliferation.	GPR39-C3	98-107	mitogen-activated protein kinase 1	Homo sapiens	59-62
31202806-0	2019	Activation of GPR39 with the agonist TC-G 1008 ameliorates ox-LDL-induced attachment of monocytes to endothelial cells.	GPR39-C3	37-46	G protein-coupled receptor 39	Homo sapiens	14-19
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	G protein-coupled receptor 39	Homo sapiens	25-30
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	interleukin 1 beta	Homo sapiens	224-241
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	interleukin 1 beta	Homo sapiens	243-251
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	interleukin 6	Homo sapiens	254-258
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	C-C motif chemokine ligand 2	Homo sapiens	264-298
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	C-C motif chemokine ligand 2	Homo sapiens	300-305
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	matrix metallopeptidase 1	Homo sapiens	356-360
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	matrix metallopeptidase 1	Homo sapiens	372-377
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	matrix metallopeptidase 3	Homo sapiens	379-384
31539553-5	2019	We found that agonism of GPR39 using its specific agonist TC-G 1008 significantly ameliorated important markers of RA, including oxidative stress, mitochondrial dysfunction, expression of proinflammatory cytokines including interleukin-1beta (IL-1beta), IL-6, and monocyte chemoattractant protein 1 (MCP-1), and secretion of key matrix metalloproteinases (MMPs) including MMP-1, MMP-3 and MMP-13.	GPR39-C3	58-67	matrix metallopeptidase 13	Homo sapiens	389-395
31448639-0	2019	GPR39 agonist TC-G 1008 promotes osteoblast differentiation and mineralization in MC3T3-E1 cells.	GPR39-C3	14-23	G protein-coupled receptor 39	Mus musculus	0-5
31448639-7	2019	Activation of GPR39 using its selective agonist TC-G 1008 induces alkaline phosphatase (ALP), osteocalcin (OCN), and type I collagen (Col-I) expression, and increases cellular ALP activity and calcium deposition, implying that GPR activation promotes cells toward osteoblast differentiation.	GPR39-C3	48-57	G protein-coupled receptor 39	Mus musculus	14-19
31448639-7	2019	Activation of GPR39 using its selective agonist TC-G 1008 induces alkaline phosphatase (ALP), osteocalcin (OCN), and type I collagen (Col-I) expression, and increases cellular ALP activity and calcium deposition, implying that GPR activation promotes cells toward osteoblast differentiation.	GPR39-C3	48-57	bone gamma-carboxyglutamate protein 2	Mus musculus	94-105
31448639-7	2019	Activation of GPR39 using its selective agonist TC-G 1008 induces alkaline phosphatase (ALP), osteocalcin (OCN), and type I collagen (Col-I) expression, and increases cellular ALP activity and calcium deposition, implying that GPR activation promotes cells toward osteoblast differentiation.	GPR39-C3	48-57	bone gamma-carboxyglutamate protein 2	Mus musculus	107-110
31448639-8	2019	Treatment with TC-G 1008 also increases Runx-2 expression and AMPK activation.	GPR39-C3	15-24	runt related transcription factor 2	Mus musculus	40-46
31448639-10	2019	These data indicate that TC-G 1008-mediated GPR39 activation involves AMPK-mediated Runx-2 induction.	GPR39-C3	25-34	G protein-coupled receptor 39	Mus musculus	44-49
31448639-10	2019	These data indicate that TC-G 1008-mediated GPR39 activation involves AMPK-mediated Runx-2 induction.	GPR39-C3	25-34	runt related transcription factor 2	Mus musculus	84-90
31237151-0	2019	GPR39 agonist TC-G 1008 ameliorates IL-1beta-induced chondrocyte senescence.	GPR39-C3	14-23	G protein-coupled receptor 39	Homo sapiens	0-5
31237151-0	2019	GPR39 agonist TC-G 1008 ameliorates IL-1beta-induced chondrocyte senescence.	GPR39-C3	14-23	interleukin 1 beta	Homo sapiens	36-44
31237151-5	2019	The GPR39 agonist TC-G 1008 mitigates IL-1beta-induced chondrocyte senescence.	GPR39-C3	18-27	G protein-coupled receptor 39	Homo sapiens	4-9
31237151-5	2019	The GPR39 agonist TC-G 1008 mitigates IL-1beta-induced chondrocyte senescence.	GPR39-C3	18-27	interleukin 1 beta	Homo sapiens	38-46
31237151-6	2019	Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53.	GPR39-C3	30-39	interleukin 1 beta	Homo sapiens	50-58
31237151-6	2019	Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53.	GPR39-C3	30-39	tumor protein p53	Homo sapiens	130-133
31237151-6	2019	Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53.	GPR39-C3	30-39	H3 histone pseudogene 16	Homo sapiens	135-138
31237151-6	2019	Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53.	GPR39-C3	30-39	serpin family E member 1	Homo sapiens	140-145
31237151-6	2019	Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53.	GPR39-C3	30-39	tumor protein p53	Homo sapiens	171-174
31237151-7	2019	Moreover, we show that TC-G 1008 treatment restores IL-1beta-induced inhibition of SIRT1 and the silencing of SIRT1 abolishes the function of TC-G 1008 on p53 acetylation and senescence, suggesting that the function of GPR39 signaling is mediated by SIRT1 in chondrocytes.	GPR39-C3	23-32	interleukin 1 beta	Homo sapiens	52-60
31237151-7	2019	Moreover, we show that TC-G 1008 treatment restores IL-1beta-induced inhibition of SIRT1 and the silencing of SIRT1 abolishes the function of TC-G 1008 on p53 acetylation and senescence, suggesting that the function of GPR39 signaling is mediated by SIRT1 in chondrocytes.	GPR39-C3	23-32	sirtuin 1	Homo sapiens	83-88
31237151-7	2019	Moreover, we show that TC-G 1008 treatment restores IL-1beta-induced inhibition of SIRT1 and the silencing of SIRT1 abolishes the function of TC-G 1008 on p53 acetylation and senescence, suggesting that the function of GPR39 signaling is mediated by SIRT1 in chondrocytes.	GPR39-C3	23-32	G protein-coupled receptor 39	Homo sapiens	219-224
31237151-7	2019	Moreover, we show that TC-G 1008 treatment restores IL-1beta-induced inhibition of SIRT1 and the silencing of SIRT1 abolishes the function of TC-G 1008 on p53 acetylation and senescence, suggesting that the function of GPR39 signaling is mediated by SIRT1 in chondrocytes.	GPR39-C3	142-151	sirtuin 1	Homo sapiens	110-115
31237151-7	2019	Moreover, we show that TC-G 1008 treatment restores IL-1beta-induced inhibition of SIRT1 and the silencing of SIRT1 abolishes the function of TC-G 1008 on p53 acetylation and senescence, suggesting that the function of GPR39 signaling is mediated by SIRT1 in chondrocytes.	GPR39-C3	142-151	tumor protein p53	Homo sapiens	155-158
31237151-7	2019	Moreover, we show that TC-G 1008 treatment restores IL-1beta-induced inhibition of SIRT1 and the silencing of SIRT1 abolishes the function of TC-G 1008 on p53 acetylation and senescence, suggesting that the function of GPR39 signaling is mediated by SIRT1 in chondrocytes.	GPR39-C3	142-151	sirtuin 1	Homo sapiens	110-115
31237151-8	2019	Altogether, our findings implicate that the activation of GPR39 signaling ameliorates IL-1beta-induced chondrocyte senescence and the GPR39 agonist TC-G 1008 could have the potential to modulate aging-associated OA.	GPR39-C3	148-157	G protein-coupled receptor 39	Homo sapiens	134-139
31202806-6	2019	Our findings show that agonism of GPR39 by the selective agonist TC-G 1008 potently reversed the effects of ox-LDL including increased expression of proinflammatory cytokines and chemokines, markers of oxidative stress, and enhanced expression of cellular adhesion molecules.	GPR39-C3	65-74	G protein-coupled receptor 39	Homo sapiens	34-39
31167986-2	2019	In a dose dependent manner and at 24 h after the elicitation by Con A, oral administration of TC-G 1008, a GPR39 agonist, reduced both, the glutamic-pyruvic transaminase levels (a marker for liver injury) and the necrosis area, as revealed by the histological analysis of tissues from mice with Con A-induced hepatitis.	GPR39-C3	94-103	G protein-coupled receptor 39	Mus musculus	107-112
31167986-3	2019	TC-G 1008 also suppressed serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha significantly at 6 h after the elicitation, suggesting that the cells producing IL-6 and/or TNF-alpha are the targets of TC-G 1008.	GPR39-C3	0-9	interleukin 6	Mus musculus	32-50
31167986-3	2019	TC-G 1008 also suppressed serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha significantly at 6 h after the elicitation, suggesting that the cells producing IL-6 and/or TNF-alpha are the targets of TC-G 1008.	GPR39-C3	0-9	tumor necrosis factor	Mus musculus	55-88
31167986-3	2019	TC-G 1008 also suppressed serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha significantly at 6 h after the elicitation, suggesting that the cells producing IL-6 and/or TNF-alpha are the targets of TC-G 1008.	GPR39-C3	0-9	interleukin 6	Mus musculus	169-173
31167986-3	2019	TC-G 1008 also suppressed serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha significantly at 6 h after the elicitation, suggesting that the cells producing IL-6 and/or TNF-alpha are the targets of TC-G 1008.	GPR39-C3	0-9	tumor necrosis factor	Mus musculus	181-190
31167986-3	2019	TC-G 1008 also suppressed serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha significantly at 6 h after the elicitation, suggesting that the cells producing IL-6 and/or TNF-alpha are the targets of TC-G 1008.	GPR39-C3	210-219	interleukin 6	Mus musculus	169-173
31167986-3	2019	TC-G 1008 also suppressed serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha significantly at 6 h after the elicitation, suggesting that the cells producing IL-6 and/or TNF-alpha are the targets of TC-G 1008.	GPR39-C3	210-219	tumor necrosis factor	Mus musculus	181-190
31167986-4	2019	One potential target cell appears to be a monocyte-derived macrophages because TC-G 1008 treatment suppressed lipopolysaccharide-induced IL-6 production from U937 macrophages in vitro.	GPR39-C3	79-88	interleukin 6	Mus musculus	137-141
31167986-5	2019	Taken together, GPR39 agonist TC-G 1008 ameliorates liver injury in the Con A model by blocking pro-inflammatory cytokine production.	GPR39-C3	30-39	G protein-coupled receptor 39	Mus musculus	16-21
30610192-7	2019	Using a drinking-in-the-dark two bottle choice (DID-2BC) model, we showed that an acute 7.5 mg/kg dose of the GPR39 agonist, TC-G 1008, reduced ethanol intake in mice without affecting total fluid intake, locomotor activity or saccharin preference.	GPR39-C3	125-134	G protein-coupled receptor 39	Mus musculus	110-115
30459126-4	2019	Treatment with TC-G 1008 (1 muM -10 muM), a GPR39 agonist, and zinc (10 muM -100 muM) increased tight junction assembly in T84 cells.	GPR39-C3	15-24	G protein-coupled receptor 39	Homo sapiens	44-49
30419533-0	2019	Long-lasting antidepressant-like activity of the GPR39 zinc receptor agonist TC-G 1008.	GPR39-C3	77-86	G protein-coupled receptor 39	Mus musculus	49-54
30419533-5	2019	BDNF protein level was evaluated in hippocampus following both acute and chronic TC-G 1008 treatment.	GPR39-C3	81-90	brain derived neurotrophic factor	Mus musculus	0-4
30419533-9	2019	We also observed some tendencies for increased BDNF following acute TC-G 1008 treatment.	GPR39-C3	68-77	brain derived neurotrophic factor	Mus musculus	47-51
30419533-10	2019	LIMITATIONS: TC-G 1008 is new drug designed to study GPR39 therefore additional pharmacodynamic and pharmacokinetic properties in preclinical studies are required.	GPR39-C3	13-22	G protein-coupled receptor 39	Mus musculus	53-58
30459126-6	2019	In addition, western blot analysis revealed that treatment with TC-G 1008 induced AMPK activation in time- and concentration-dependent manners.	GPR39-C3	64-73	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	82-86
30459126-7	2019	Interestingly, inhibitors of phospholipase C (PLC) and calcium/calmodulin-dependent protein kinase kinase beta (CaMKKbeta) abrogated the effect of TC-G 1008 on inducing AMPK activation, tight junction assembly and zonula occludens-1 re-organization.	GPR39-C3	147-156	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	112-121
30459126-7	2019	Interestingly, inhibitors of phospholipase C (PLC) and calcium/calmodulin-dependent protein kinase kinase beta (CaMKKbeta) abrogated the effect of TC-G 1008 on inducing AMPK activation, tight junction assembly and zonula occludens-1 re-organization.	GPR39-C3	147-156	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	169-173
30053407-3	2018	TC-G 1008, a G protein-coupled receptor 39 agonist, enhanced interleukin (IL)-10 production from thioglycollate-induced peritoneal macrophages stimulated with lipopolysaccharide (LPS) in vitro.	GPR39-C3	0-9	G protein-coupled receptor 39	Mus musculus	13-42
30053407-3	2018	TC-G 1008, a G protein-coupled receptor 39 agonist, enhanced interleukin (IL)-10 production from thioglycollate-induced peritoneal macrophages stimulated with lipopolysaccharide (LPS) in vitro.	GPR39-C3	0-9	interleukin 10	Mus musculus	61-80
30053407-4	2018	In addition, the oral administration of TC-G 1008 enhanced serum IL-10 concentrations in an LPS-induced murine model of sepsis.	GPR39-C3	40-49	interleukin 10	Mus musculus	65-70
30053407-5	2018	The ablation of G protein-coupled receptor 39 significantly reduced IL-10 production by TC-G 1008 in thioglycollate-induced peritoneal macrophages stimulated with LPS and in the LPS-induced murine model of sepsis.	GPR39-C3	88-97	G protein-coupled receptor 39	Mus musculus	16-45
30053407-5	2018	The ablation of G protein-coupled receptor 39 significantly reduced IL-10 production by TC-G 1008 in thioglycollate-induced peritoneal macrophages stimulated with LPS and in the LPS-induced murine model of sepsis.	GPR39-C3	88-97	interleukin 10	Mus musculus	68-73