PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10686508-3	2000	In the present study, we investigated the effect of sodium salicylate (NaSal), a nonsteroidal anti-inflammatory drug, on mitogen-activated protein kinases (MAPK) and apoptosis of human eosinophils.	Sodium Salicylate	52-69	mitogen-activated protein kinase 1	Homo sapiens	156-160	
16393981-6	2006	For example, sodium salicylate blocked GM-CSF-stimulated Erk and Akt activation, but resulted in rapid and sustained activation of p38-MAPK, an event mimicked by okadaic acid that also accelerates Mcl-1 turnover and neutrophil apoptosis.	Sodium Salicylate	13-30	mitogen-activated protein kinase 1	Homo sapiens	57-60	
10574634-4	1999	In contrast, sodium salicylate (NaSal), a nonsteroidal anti-inflammatory drug (NSAID), could activate p38 MAPK but not ERK within one hour.	Sodium Salicylate	13-30	mitogen-activated protein kinase 1	Homo sapiens	119-122	
10574634-4	1999	In contrast, sodium salicylate (NaSal), a nonsteroidal anti-inflammatory drug (NSAID), could activate p38 MAPK but not ERK within one hour.	Sodium Salicylate	32-37	mitogen-activated protein kinase 1	Homo sapiens	119-122	
9826736-4	1998	Exposure of neutrophils to aspirin or sodium salicylate (poor COX inhibitor) inhibited Erk activity and adhesiveness of formylmethionyl-leucyl-phenylalanine- and arachidonic acid-stimulated neutrophils, consistent with anti-inflammation but not COX inhibition (IC50s = 1-8 mM).	Sodium Salicylate	38-55	mitogen-activated protein kinase 1	Homo sapiens	87-90