PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19224363-4	2009	7-Ketocholesterol induced the nuclear damage, loss of the mitochondrial transmembrane potential, increase in the cytosolic Bax and cytochrome c levels, caspase-3 activation and cell death in differentiated PC12 cells.	7-ketocholesterol	0-17	caspase 3	Rattus norvegicus	152-161	
19224363-5	2009	Glycyrrhizin and 18beta-glycyrrhetinic acid prevented the 7-ketocholesterol-induced mitochondrial damage, leading to caspase-3 activation and cell death.	7-ketocholesterol	58-75	caspase 3	Rattus norvegicus	117-126	
16715209-2	2006	7-Ketocholesterol significantly enhanced the MPP(+)-induced nuclear damage, decrease in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive oxygen species and depletion of GSH.	7-ketocholesterol	0-17	caspase 3	Rattus norvegicus	185-194	
21035514-4	2011	7-Ketocholesterol induced a decrease in cytosolic Bid and Bcl-2 levels, increase in cytosolic Bax levels, cytochrome c release, caspase-3 activation and upregulation of p53.	7-ketocholesterol	0-17	caspase 3	Rattus norvegicus	128-137	
19957203-3	2010	Tyrphostin AG126 significantly attenuated the 7-ketocholesterol-induced decrease in cytosolic Bid and Bcl-2 levels, increase in cytosolic pro-apoptotic Bax levels, mitochondrial membrane potential loss, cytochrome c release and subsequent caspase-3 activation.	7-ketocholesterol	46-63	caspase 3	Rattus norvegicus	239-248	
19957203-5	2010	The results show that tyrphostin AG126 may prevent the 7-ketocholesterol toxicity by suppressing the mitochondrial membrane permeability change that leads to the cytochrome c release and caspase-3 activation.	7-ketocholesterol	55-72	caspase 3	Rattus norvegicus	187-196	
17224136-3	2007	PC12 cells exposed to 7-ketocholesterol revealed nuclear damage, decrease in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive oxygen species and depletion of GSH.	7-ketocholesterol	22-39	caspase 3	Rattus norvegicus	174-183	
17224136-6	2007	The results suggest that calmodulin antagonists may prevent the 7-ketocholesterol-induced viability loss in PC12 cells by suppressing formation of the mitochondrial permeability transition, leading to the release of cytochrome c and subsequent activation of caspase-3.	7-ketocholesterol	64-81	caspase 3	Rattus norvegicus	258-267	
17151911-2	2007	Calmodulin antagonists calmidazolium and W-7 prevented the 7-ketocholesterol-induced mitochondrial damage, leading to caspase-3 activation and cell death, whereas Ca2+ channel blocker nicardipine, mitochondrial Ca2+ uptake inhibitor ruthenium red, and cell permeable Ca2+ chelator BAPTA-AM did not reduce it.	7-ketocholesterol	59-76	caspase 3	Rattus norvegicus	118-127	
16715209-5	2006	7-Ketocholesterol may enhance the MPP(+)-induced viability loss in PC12 cells by promoting the mitochondrial membrane permeability change, release of cytochrome c and subsequent activation of caspase-3, which is associated with the increased formation of reactive oxygen species and depletion of GSH.	7-ketocholesterol	0-17	caspase 3	Rattus norvegicus	192-201