PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19298531-13	2009	Phosphorylation of extracellular signal-regulated kinase 2, p38 and c-Jun N-terminal kinase 1 was significantly reversed in the LV of EGCG-treated TAC rats (40%, 53% and 52% vs TAC, respectively), accompanied by significant inhibition of nuclear factor-kappaB and activator protein-1.	epigallocatechin gallate	134-138	mitogen-activated protein kinase 8	Rattus norvegicus	68-93	
24307060-2	2014	This study aimed to determine whether EGCG protects against regional myocardial ischemia/reperfusion (I/R) injuries and its underlying mechanisms involving the role of reperfusion injury salvage kinase (RISK) pathways (PI3K-Akt and ERK 1/2) and GSK-3beta or apoptotic kinases (p38 and JNK).	epigallocatechin gallate	38-42	mitogen-activated protein kinase 8	Rattus norvegicus	285-288	
24307060-10	2014	EGCG significantly enhanced the phosphorylation of Akt and GSK-3beta but not ERK1/2, while it reduced that of p38 and JNK.	epigallocatechin gallate	0-4	mitogen-activated protein kinase 8	Rattus norvegicus	118-121	
24307060-11	2014	These results suggest that EGCG has a protective effect against regional myocardial I/R injuries through activation of the RISK pathway and attenuation of p38 and JNK.	epigallocatechin gallate	27-31	mitogen-activated protein kinase 8	Rattus norvegicus	163-166	
24050715-5	2013	The mechanism of this protective effect seems to be related to: (a) the ability of EGCG to preserve the mitochondrial function and thus to prevent the TCDD-induced inhibition of glucose-stimulated insulin secretion and (b) the ability of EGCG to inhibit the TCDD-induced activation of selected kinases, such as e.g. ERK 1/2 and JNK.	epigallocatechin gallate	238-242	mitogen-activated protein kinase 8	Rattus norvegicus	328-331	
20798525-12	2010	EGCG (40muM) activated the time-dependent phosphorylated Erk, JNK and p38 MAPK.	epigallocatechin gallate	0-4	mitogen-activated protein kinase 8	Rattus norvegicus	62-65	
11791013-6	2002	In RAoSMCs, EGCG dramatically inhibited Ras activation and c-jun N-terminal kinase (JNK) activity without affecting protein kinase C expression.	epigallocatechin gallate	12-16	mitogen-activated protein kinase 8	Rattus norvegicus	59-82	
17079869-6	2006	The EGCG pretreatment inhibits the Ang II-induced phosphorylation of ERK 1/2, JNK 1/2, or p38 MAPK, and the expression of c-jun or c-fos mRNA.	epigallocatechin gallate	4-8	mitogen-activated protein kinase 8	Rattus norvegicus	78-81	
11791013-6	2002	In RAoSMCs, EGCG dramatically inhibited Ras activation and c-jun N-terminal kinase (JNK) activity without affecting protein kinase C expression.	epigallocatechin gallate	12-16	mitogen-activated protein kinase 8	Rattus norvegicus	84-87	
11791013-8	2002	These results indicate that the anti-proliferative effect of EGCG on RAoSMCs is partly Ras/JNK mediated, independent of protein kinase C, and is attributable to the downregulation of c-jun expression.	epigallocatechin gallate	61-65	mitogen-activated protein kinase 8	Rattus norvegicus	91-94	
29107025-7	2017	A-type-EGCG-dimer and pioglitazone reduced the expression levels of the GRP78, PEPCK, G6Pase, p-PERK, p-IRE1, p-JNK, ATF4, CHOP and increased p-AKT in livers of the Pb group.	epigallocatechin gallate	7-11	mitogen-activated protein kinase 8	Rattus norvegicus	112-115	
27306149-11	2016	In conclusion, epigallocatechin-3-O-gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti-inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP-1 pathway.	epigallocatechin gallate	15-43	mitogen-activated protein kinase 8	Rattus norvegicus	210-213	
27306149-11	2016	In conclusion, epigallocatechin-3-O-gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti-inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP-1 pathway.	epigallocatechin gallate	45-49	mitogen-activated protein kinase 8	Rattus norvegicus	210-213	
25422948-7	2014	EGCG significantly inhibited the expression of pro-inflammatory mediators and matrix metalloproteinases in vitro, as well as radiculopathic pain in vivo, most probably by modulation of the activity of IRAK-1 and its downstream effectors p38, JNK and NF-kappaB.	epigallocatechin gallate	0-4	mitogen-activated protein kinase 8	Rattus norvegicus	242-245