PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32376896-6	2020	In addition, catechol suppressed EMT-related steps such as migration, invasion, anoikis resistance acquisition, and stem cell-like characterization through the EGFR-AKT-ERK signaling pathway during liver cancer metastasis.	catechol	13-21	mitogen-activated protein kinase 1	Homo sapiens	169-172	
27167001-0	2016	A natural small molecule, catechol, induces c-Myc degradation by directly targeting ERK2 in lung cancer.	catechol	26-34	mitogen-activated protein kinase 1	Homo sapiens	84-88	
27167001-5	2016	Catechol inhibited ERK2 kinase activity in vitro, and its direct binding to the ERK2 active site was confirmed by X-ray crystallography.	catechol	0-8	mitogen-activated protein kinase 1	Homo sapiens	19-23	
27167001-5	2016	Catechol inhibited ERK2 kinase activity in vitro, and its direct binding to the ERK2 active site was confirmed by X-ray crystallography.	catechol	0-8	mitogen-activated protein kinase 1	Homo sapiens	80-84	
27167001-6	2016	Phosphorylation of c-Myc, a substrate of ERK2, was decreased in catechol-treated lung cancer cells and resulted in reduced protein stability and subsequent down-regulation of total c-Myc.	catechol	64-72	mitogen-activated protein kinase 1	Homo sapiens	41-45	
27167001-9	2016	In summary, catechol exerted inhibitory effects on the ERK2/c-Myc signaling axis to reduce lung cancer tumor growth in vitro and in vivo, including a preclinical patient-derived xenograft (PDX) model.	catechol	12-20	mitogen-activated protein kinase 1	Homo sapiens	55-59	
25122505-10	2014	Exposure of platelets to catechol decreased AA-induced ERK and p38 phosphorylation.	catechol	25-33	mitogen-activated protein kinase 1	Homo sapiens	55-58	
25122505-10	2014	Exposure of platelets to catechol decreased AA-induced ERK and p38 phosphorylation.	catechol	25-33	mitogen-activated protein kinase 1	Homo sapiens	63-66	
25122505-12	2014	These results suggest that catechol exhibited anti-platelet and anti-inflammatory effects, which were mediated by inhibition of COX, ROS and TXA2 production as well as ERK/p38 phosphorylation.	catechol	27-35	mitogen-activated protein kinase 1	Homo sapiens	168-171	
25122505-12	2014	These results suggest that catechol exhibited anti-platelet and anti-inflammatory effects, which were mediated by inhibition of COX, ROS and TXA2 production as well as ERK/p38 phosphorylation.	catechol	27-35	mitogen-activated protein kinase 1	Homo sapiens	172-175	
25122505-0	2014	Antiplatelet effect of catechol is related to inhibition of cyclooxygenase, reactive oxygen species, ERK/p38 signaling and thromboxane A2 production.	catechol	23-31	mitogen-activated protein kinase 1	Homo sapiens	101-104	
25122505-0	2014	Antiplatelet effect of catechol is related to inhibition of cyclooxygenase, reactive oxygen species, ERK/p38 signaling and thromboxane A2 production.	catechol	23-31	mitogen-activated protein kinase 1	Homo sapiens	105-108	
15901486-9	2005	A pharmacological inhibitor of ERK aggravated the 4-OHE2-induced cytotoxicity, supporting the pivotal role of ERK in protecting against catechol estrogen-induced oxidative cell death.	catechol	136-144	mitogen-activated protein kinase 1	Homo sapiens	31-34	
15901486-9	2005	A pharmacological inhibitor of ERK aggravated the 4-OHE2-induced cytotoxicity, supporting the pivotal role of ERK in protecting against catechol estrogen-induced oxidative cell death.	catechol	136-144	mitogen-activated protein kinase 1	Homo sapiens	110-113