PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	
31237151-5	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	
31237151-7	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	
31237151-8	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	
31202806-0	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	
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	
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	
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	
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