PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21424111-5	2011	Bisphosphonates markedly induced caspase-3 activaion, which was diminished in cells exposed to APC.	Diphosphonates	0-15	caspase 3	Homo sapiens	33-42	
25894100-7	2016	All BPs, except etidronate, were cytotoxic, as indicated by increased caspase-3/7 activity and numbers of Annexin-fluorescein isothiocyanate positive cells in ESCC cell lines.	Diphosphonates	4-7	caspase 3	Homo sapiens	70-79	
25496233-8	2014	RESULTS: Treatment of MDA-MB-231 with BP induced caspase 3/7 activity, with zoledronic acid being the most effective.	Diphosphonates	38-40	caspase 3	Homo sapiens	49-58	
25496233-10	2014	Co-treatment with probenecid enhanced BP effects on cell viability, IPP/ApppI accumulation as measurable in MCF-7 and T47D cells, caspase 3/7 activity and target gene expression.	Diphosphonates	38-40	caspase 3	Homo sapiens	130-139	
25496233-12	2014	CONCLUSIONS: In summary, we demonstrate effects of various bisphosphonates on caspase 3/7 activity, cell viability and expression of tumor suppressor genes in breast cancer cells.	Diphosphonates	59-74	caspase 3	Homo sapiens	78-87	
23381659-7	2013	S1P blocked BP-induced caspase-3 activation, nuclear factor-kappaB activation, c-Jun-N-terminal kinase (JNK) phosphorylation and DNA fragmentation.	Diphosphonates	12-14	caspase 3	Homo sapiens	23-32	
21424111-8	2011	In conclusion, the present study demonstrates that APC inhibits bisphosphonate-induced endothelial cell death via EPCR-induced inactivation of caspase-3 and NF-kappaB, and also suggests that APC has the potential to be a therapeutic drug in various vascular diseases induced by endothelial cell damage.	Diphosphonates	64-78	caspase 3	Homo sapiens	143-152	
11344045-8	2001	Caspase-3, therefore, appears to be the major effector caspase activated in osteoclasts by bisphosphonate treatment.	Diphosphonates	91-105	caspase 3	Homo sapiens	0-9	
21297379-5	2011	The cells showed no response to TRAIL alone; however, pre-treatment with bisphosphonates significantly increased TRAIL-mediated apoptosis and cellular activation of caspase-3.	Diphosphonates	73-88	caspase 3	Homo sapiens	165-174	
11344045-0	2001	Visualization of bisphosphonate-induced caspase-3 activity in apoptotic osteoclasts in vitro.	Diphosphonates	17-31	caspase 3	Homo sapiens	40-49	
11344045-6	2001	Bisphosphonate-induced osteoclast apoptosis was dependent on caspase activation, because apoptosis resulting from alendronate, clodronate, or zoledronic acid treatment was suppressed by zVAD-fmk, a broad-range caspase inhibitor, or by SB-281277, a specific isatin sulfonamide inhibitor of caspase-3/-7.	Diphosphonates	0-14	caspase 3	Homo sapiens	289-301	
31423185-9	2019	Additionally, BPs were revealed to induce reactive oxygen species expression, caspase-3 activity and increase the mitochondrial transmembrane potential, which was associated with apoptosis.	Diphosphonates	14-17	caspase 3	Homo sapiens	78-87	
31423185-10	2019	BP-induced cancer cell apoptosis was detected by acridine orange/ethidium bromide staining and flow cytometry analysis, and was identified to be associated with the induction of caspase-3 and cytochrome c protein expression.	Diphosphonates	0-2	caspase 3	Homo sapiens	178-187