PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26689473-4	2016	It remains to identify the link between ERK/Akt up-regulation and the consequent quenching effect on ROS intracellular level that efficiently and markedly delay the pro-apoptotic effect of the oxysterol.	Oxysterols	193-202	mitogen-activated protein kinase 1	Homo sapiens	40-43	
21359969-0	2011	Lanthanum chloride suppresses oxysterol-induced ECV-304 cell apoptosis via inhibition of intracellular Ca(2+) concentration elevation, oxidative stress, and activation of ERK and NF-kappaB signaling pathways.	Oxysterols	30-39	mitogen-activated protein kinase 1	Homo sapiens	171-174	
19157829-4	2010	Moreover, the carotenoid strongly prevented the increase of NOX-4, hsp70 and hsp90 expressions as well as the phosphorylation of the redox-sensitive p38, JNK and ERK1/2 induced by the oxysterol.	Oxysterols	184-193	mitogen-activated protein kinase 1	Homo sapiens	149-152	
16214031-5	2005	Up-regulated expression and synthesis of MCP-1 by the oxysterol mixture was clearly dependent on a net increment of phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor kappaB (NF-kappaB) nuclear binding.	Oxysterols	54-63	mitogen-activated protein kinase 1	Homo sapiens	135-176	
15788406-0	2005	Oxysterols inhibit phosphatidylcholine synthesis via ERK docking and phosphorylation of CTP:phosphocholine cytidylyltransferase.	Oxysterols	0-10	mitogen-activated protein kinase 1	Homo sapiens	53-56	
14992685-10	2004	The oxysterol also inhibited (i) the histamine- and thapsigargin-induced arachidonic acid release, and (ii) the phosphorylation of both cPLA2 and ERK1/2 (extracellular-signal-regulated kinases 1/2).	Oxysterols	4-13	mitogen-activated protein kinase 1	Homo sapiens	154-196	
26689473-6	2016	The 27-OH-exerted induction of Nrf2 and subsequently of the target genes, HO-1 and NQO-1, was proved to be: (i) dependent upon the activation of ERK and Akt pathways, (ii) directly responsible for the quenching of intracellular oxidative stress and by this way (iii) ultimately responsible for the observed oxysterol-induced pro-survival response.	Oxysterols	307-316	mitogen-activated protein kinase 1	Homo sapiens	145-148	
25736858-4	2015	p38 MAPK activation plays a major role, while other signal branches, i.e. the JNK and ERK pathways, make minor contributions to the intestinal inflammation induced by dietary oxysterols.	Oxysterols	175-185	mitogen-activated protein kinase 1	Homo sapiens	86-89	
25110320-3	2014	A net up-regulation of survival signaling, involving the extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/Akt phosphorylation pathways, was observed in U937 promonocytic cells cultivated over time in the presence of a low micromolar concentration of the oxysterol.	Oxysterols	286-295	mitogen-activated protein kinase 1	Homo sapiens	57-94	
25110320-5	2014	In turn, stimulation of ERK and PI3K/Akt both significantly quenched ROS steady state and markedly phosphorylated Bad, thereby determining a marked delay of the oxysterol s proapoptotic action.	Oxysterols	161-170	mitogen-activated protein kinase 1	Homo sapiens	24-27