PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22806078-2	2013	In so-called type II cells, an additional mechanism involving tBid-mediated caspase-9 activation is required to efficiently trigger cell death.	tBID	62-66	caspase 9	Homo sapiens	76-85	
23834359-5	2013	We show that caspase-9 can cleave Bid into tBid at amino acid 59 and that this cleavage of Bid is required for ROS production following serum withdrawal.	tBID	43-47	caspase 9	Homo sapiens	13-22	
23834359-8	2013	CONCLUSIONS: Taken together, these data suggest that caspase-9 is required for mitochondrial morphological changes and ROS production by cleaving and activating Bid into tBid.	tBID	170-174	caspase 9	Homo sapiens	53-62	
12519725-6	2003	Studies with Apaf-1- and caspase-9-deficient primary MEFs indicated that both proteins were essential for nc/wtBID and for tBID-induced apoptosis.	tBID	110-114	caspase 9	Homo sapiens	25-34	
12154014-3	2002	The active truncated form of BID (tBID) triggers the mitochondrial activation of caspase-9 by inducing the activation of BAK or BAX.	tBID	34-38	caspase 9	Homo sapiens	81-90	
10949027-3	2000	Rather, TNF-alpha induced a tBid-dependent conformational change in Bax that allowed an interaction between E1B 19K and conformationally altered Bax, which caused inhibition of cytochrome c release and caspase-9 activation.	tBID	28-32	caspase 9	Homo sapiens	202-211