PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30140376-5	2018	STK405759 combined with dexamethasone or bortezomib had synergistic cytotoxic activity in RPMIS, CAG and MM1.S human MM cell lines through activation of caspase 2, 3, 8, 9 and PARP.	Bortezomib	41-51	caspase 2	Homo sapiens	153-171	
16446371-5	2006	PS-341 disrupted lysosomes with redistribution of cathepsin B to the cytosol, as shown using fluorescence confocal microscopy, that was blocked by the free radical scavenger tiron but not by a caspase-2 inhibitor (benzyloxycarbonyl (Z)-VDVAD-fluoromethyl ketone (FMK)).	Bortezomib	0-6	caspase 2	Homo sapiens	193-202	
16446371-6	2006	PS-341-induced caspase-2 activation was attenuated by a selective pharmacological inhibitor of cathepsin B (R-3032), suggesting that cathepsin B release occurs upstream of caspase-2.	Bortezomib	0-6	caspase 2	Homo sapiens	15-24	
16446371-6	2006	PS-341-induced caspase-2 activation was attenuated by a selective pharmacological inhibitor of cathepsin B (R-3032), suggesting that cathepsin B release occurs upstream of caspase-2.	Bortezomib	0-6	caspase 2	Homo sapiens	172-181	
16446371-11	2006	Taken together, PS-341 induces lysosomal cathepsin B redistribution upstream of caspase-2.	Bortezomib	16-22	caspase 2	Homo sapiens	80-89	
16446371-12	2006	Caspase-2 activation regulates PS-341-induced mitochondrial depolarization and apoptosis, suggesting that caspase-2 can serve as a link between lysosomal and mitochondrial permeabilization.	Bortezomib	31-37	caspase 2	Homo sapiens	0-9	
16446371-12	2006	Caspase-2 activation regulates PS-341-induced mitochondrial depolarization and apoptosis, suggesting that caspase-2 can serve as a link between lysosomal and mitochondrial permeabilization.	Bortezomib	31-37	caspase 2	Homo sapiens	106-115	
18723477-0	2008	Caspase-2 functions upstream of mitochondria in endoplasmic reticulum stress-induced apoptosis by bortezomib in human myeloma cells.	Bortezomib	98-108	caspase 2	Homo sapiens	0-9	
18723477-5	2008	Using caspase inhibitors and a RNA interference approach, we finally confirmed that bortezomib-triggered apoptosis in multiple myeloma cells is dependent on caspase-2 activation, which is associated with ER stress and required for release of cytochrome c, breakdown of mitochondrial transmembrane potential, and its downstream caspase-9 activation.	Bortezomib	84-94	caspase 2	Homo sapiens	6-13	
18723477-5	2008	Using caspase inhibitors and a RNA interference approach, we finally confirmed that bortezomib-triggered apoptosis in multiple myeloma cells is dependent on caspase-2 activation, which is associated with ER stress and required for release of cytochrome c, breakdown of mitochondrial transmembrane potential, and its downstream caspase-9 activation.	Bortezomib	84-94	caspase 2	Homo sapiens	157-166	
18723477-6	2008	Taken together, these data strongly suggest that caspase-2 can serve as a proximal caspase that functions upstream of mitochondrial signaling during ER stress-induced apoptosis by bortezomib in multiple myeloma cells.	Bortezomib	180-190	caspase 2	Homo sapiens	49-58	
18723477-6	2008	Taken together, these data strongly suggest that caspase-2 can serve as a proximal caspase that functions upstream of mitochondrial signaling during ER stress-induced apoptosis by bortezomib in multiple myeloma cells.	Bortezomib	180-190	caspase 2	Homo sapiens	49-56	
16446371-0	2006	PS-341 (bortezomib) induces lysosomal cathepsin B release and a caspase-2-dependent mitochondrial permeabilization and apoptosis in human pancreatic cancer cells.	Bortezomib	0-6	caspase 2	Homo sapiens	64-73	
16446371-0	2006	PS-341 (bortezomib) induces lysosomal cathepsin B release and a caspase-2-dependent mitochondrial permeabilization and apoptosis in human pancreatic cancer cells.	Bortezomib	8-18	caspase 2	Homo sapiens	64-73	
16446371-4	2006	PS-341 induced a dose-dependent apoptosis in association with reactive oxygen species generation and cleavage of caspase-2 to its 33- and 14-kDa fragments.	Bortezomib	0-6	caspase 2	Homo sapiens	113-122