PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16628188-6	2006	The mechanism of cell killing was via PTL-induced generation of reactive oxygen species, resulting in turn in a proapoptotic Bax conformational change, release of mitochondrial cytochrome c and caspase activation.	parthenolide	38-41	cytochrome c, somatic	Homo sapiens	177-189	
19659784-9	2009	PAR-induced apoptosis was associated with intracellular events including the decline of mitochondrial potential, increased release of cytochrome C from the mitochondria, decreased expression of Bcl-2, increased expression of Bax, Bid and tBid and activation of caspase 3 and 8.	parthenolide	0-3	cytochrome c, somatic	Homo sapiens	134-146	
19067767-2	2009	We also found that parthenolide could target IKK activity and then inhibit NF-kappaB; this promoted cytochrome c release and activation of caspases 3 and 9.	parthenolide	19-31	cytochrome c, somatic	Homo sapiens	100-112	
25370819-7	2015	In addition SAHA/PN combination induced GSH depletion, fall in Deltapsim, release of cytochrome c, activation of caspase 3 and apoptosis.	parthenolide	17-19	cytochrome c, somatic	Homo sapiens	85-97	
15286701-7	2004	Cytochrome c but not Smac/DIABLO was released from the mitochondria in cells treated with parthenolide alone.	parthenolide	90-102	cytochrome c, somatic	Homo sapiens	0-12	
15219941-7	2004	All these alterations were found to be prerequisite for the subsequent release of proapopototic mitochondrial proteins, including cytochrome c and Samc, in parthenolide-treated cells.	parthenolide	156-168	cytochrome c, somatic	Homo sapiens	130-142	
27122844-7	2015	RESULTS: Parthenolide caused apoptosis at 30 mu M, as judged by TUNEL assay and Bax and cytochrome c translocation.	parthenolide	9-21	cytochrome c, somatic	Homo sapiens	88-100