PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
9795219-7	1998	Caspase-3 activation and morphological changes were prevented by cycloheximide treatment.	Cycloheximide	65-78	caspase 3	Mus musculus	0-9	
22721505-9	2012	MODE-K cells are sensitive to TNF-alpha-induced apoptosis in the presence of CHX, which is associated with increased intracellular ROS production and caspase-3/7 activation.	Cycloheximide	77-80	caspase 3	Mus musculus	150-159	
17295206-8	2007	Genistein plus zinc-induced increase in caspase-3 mRNA expression was completely inhibited in the presence of cycloheximide (10(-7) M), an inhibitor of protein synthesis, or 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB; 10(-6) M), an inhibitor of transcription activity.	Cycloheximide	110-123	caspase 3	Mus musculus	40-49	
35279675-6	2022	In vitro, treatment with tumour necrosis factor-alpha (TNF-alpha) plus cycloheximide (CHX) or SLE sera induced HK2 cells to undergo pyroptosis in a caspase-3- and GSDME-dependent manner.	Cycloheximide	71-84	caspase 3	Mus musculus	148-157	
27739412-4	2016	Co-treatment with cycloheximide expedited apoptosis induction in necrostatin-1/TNF-treated L929 cells: typical apoptotic morphological changes, including membrane blebbing and nuclear fragmentation, induction of caspase-3 activity, proteolytic activation of caspases-3, -8, and -9, and cleavage of poly(ADP-ribose) polymerase (PARP) (a well-known substrate of caspase-3) were observed.	Cycloheximide	18-31	caspase 3	Mus musculus	212-221	
27739412-4	2016	Co-treatment with cycloheximide expedited apoptosis induction in necrostatin-1/TNF-treated L929 cells: typical apoptotic morphological changes, including membrane blebbing and nuclear fragmentation, induction of caspase-3 activity, proteolytic activation of caspases-3, -8, and -9, and cleavage of poly(ADP-ribose) polymerase (PARP) (a well-known substrate of caspase-3) were observed.	Cycloheximide	18-31	caspase 3	Mus musculus	258-280	
27739412-4	2016	Co-treatment with cycloheximide expedited apoptosis induction in necrostatin-1/TNF-treated L929 cells: typical apoptotic morphological changes, including membrane blebbing and nuclear fragmentation, induction of caspase-3 activity, proteolytic activation of caspases-3, -8, and -9, and cleavage of poly(ADP-ribose) polymerase (PARP) (a well-known substrate of caspase-3) were observed.	Cycloheximide	18-31	caspase 3	Mus musculus	360-369	
18636177-8	2008	CRP plus zinc-induced increase in caspase-3 mRNA expression was completely inhibited in the presence of cycloheximide (10(-7) M), an inhibitor of protein synthesis, or 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DBR; 10(-6) M), an inhibitor of transcription activity.	Cycloheximide	104-117	caspase 3	Mus musculus	34-43	
15808420-8	2005	TG induced elevated ROS levels and suppressed caspase-3 in apoptotic cells pretreated for 24 h with cycloheximide.	Cycloheximide	100-113	caspase 3	Mus musculus	46-55