PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11228543-0	2000	Aspirin induces apoptosis through release of cytochrome c from mitochondria.	Aspirin	0-7	cytochrome c, somatic	Homo sapiens	45-57	
19706045-7	2009	RESULTS: In these MSCs, aspirin induced morphological changes characteristic of apoptosis, cytochrome c release from mitochondria, and caspase-3 activation.	Aspirin	24-31	cytochrome c, somatic	Homo sapiens	91-103	
19706045-8	2009	Stimulating the Wnt/beta-catenin pathway by both Wnt 3a and GSK-3beta inhibitors (LiCl and SB 216763), blocked aspirin-induced apoptosis and protected mitochondrial function, as demonstrated by decreased cytochrome c release and caspase-3 activity.	Aspirin	111-118	cytochrome c, somatic	Homo sapiens	204-216	
15579484-7	2005	We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release.	Aspirin	15-22	cytochrome c, somatic	Homo sapiens	162-174	
15546508-3	2004	ASA and indomethacin triggered apoptosis in cells of all three lines through release of cytosolic cytochrome c, activation of caspase-9 and-3, and cleavage of poly(ADP-ribose) polymerase (PARP), but NS398 induced minimal apoptosis only in Ishikawa cells.	Aspirin	0-3	cytochrome c, somatic	Homo sapiens	98-110	
11228543-5	2000	The release of cytochrome c from mitochondria was inhibited by overexpression of the antiapoptotic protein Bcl-2 and cells that lack Apaf-1 were resistant to aspirin-induced apoptosis.	Aspirin	158-165	cytochrome c, somatic	Homo sapiens	15-27	
11228543-6	2000	These data provide evidence that the release of cytochrome c is an important part of the apoptotic mechanism of aspirin.	Aspirin	112-119	cytochrome c, somatic	Homo sapiens	48-60	
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	cytochrome c, somatic	Homo sapiens	156-168	
11034327-0	2000	Aspirin induces apoptosis through mitochondrial cytochrome c release.	Aspirin	0-7	cytochrome c, somatic	Homo sapiens	48-60	
11034327-4	2000	The apoptotic effect of aspirin was analyzed in different cell lines (Jurkat, MOLT-4, Raji and HL-60) showing induction of mitochondrial cytochrome c release and caspases 9, 3 and 8 processing.	Aspirin	24-31	cytochrome c, somatic	Homo sapiens	137-149	
11034327-5	2000	Furthermore, early aspirin-induced cytochrome c release was not affected by the caspase inhibitor Z-VAD x fmk and preceded loss of mitochondrial membrane potential.	Aspirin	19-26	cytochrome c, somatic	Homo sapiens	35-47	
11034327-6	2000	Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release.	Aspirin	11-18	cytochrome c, somatic	Homo sapiens	73-85	
21722632-7	2011	ASA increased the production of reactive oxygen species, reduced the cellular glutathione (GSH) pool and inhibited the activities of the mitochondrial respiratory enzyme complexes, NADH-ubiquinone oxidoreductase (complex I), cytochrome c oxidase (complex IV) and the mitochondrial matrix enzyme, aconitase.	Aspirin	0-3	cytochrome c, somatic	Homo sapiens	225-237	
25596165-5	2015	Kinetics study revealed that the modification of cytochrome c with BAMF took place at faster rates than aspirin.	Aspirin	104-111	cytochrome c, somatic	Homo sapiens	49-61	
23611778-5	2013	We further showed that aspirin robustly enhanced Navitoclax-triggered cytosolic cytochrome c release, activation of initiator caspase-9 and effector caspase-3, and cleavage of PARP.	Aspirin	23-30	cytochrome c, somatic	Homo sapiens	80-92