PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27807662-6	2017	Sorafenib plus C2-ceramide stimulated significantly the production of reactive oxygen species (ROS) and mitochondrial depolarization, which promoted caspases-dependent cell apoptosis as illustrated by related protein expression including caspase 3, caspase 9, Bax, Bcl-2, and cytochrome c.	Sorafenib	0-9	cytochrome c, somatic	Homo sapiens	276-288	
30522045-3	2019	This study aimed to investigate the involvement of mitochondrial cytochrome c-dependent apoptosis in the mechanism of action of a combination of paclitaxel, sorafenib, and RT in RCC and breast cancer.	Sorafenib	157-166	cytochrome c, somatic	Homo sapiens	65-77	
24366851-2	2014	In MOGGCCM cells, sorafenib initiated mainly apoptosis, mediated by the mitochondrial pathway with mitochondrial membrane permeabilization, cytochrome c release to the cytoplasm, and activation of caspase 9 and 3.	Sorafenib	18-27	cytochrome c, somatic	Homo sapiens	140-152	
26097873-7	2015	The sorafenib-increased cathepsin B activity induced the proteolysis of Bid into tBid that stimulates the intrinsic pathway of apoptosis characterized by mitochondrial membrane depolarization, oxygen radical generation and cytochrome c release.	Sorafenib	4-13	cytochrome c, somatic	Homo sapiens	223-235	
26516583-8	2015	In addition, signs of both caspase-dependent and - independent apoptosis were observed, as cotreatment with FTY720 and sorafenib caused cytochrome c release and poly-ADP ribose polymerase-cleavage as well as translocation of Apoptosis-inducing factor into the cytosol.	Sorafenib	119-128	cytochrome c, somatic	Homo sapiens	136-148	
23384035-4	2013	Using RPMI8226 cells co-expressing histone 2B-mCherry and cytochrome c-GFP, bortezomib- and sorafenib-induced apoptosis was confirmed, and both agents combined showed synergism.	Sorafenib	92-101	cytochrome c, somatic	Homo sapiens	58-70	
23108376-4	2013	Exposure of cells or isolated mitochondria to sorafenib substantially induces cytochrome c release.	Sorafenib	46-55	cytochrome c, somatic	Homo sapiens	78-90	
17909059-4	2007	Sorafenib/TRAIL-induced cell death was accompanied by mitochondrial injury and release of cytochrome c, Smac, and AIF into the cytosol and caspase-9, caspase-3, caspase-7, and caspase-8 activation.	Sorafenib	0-9	cytochrome c, somatic	Homo sapiens	90-102	
20197401-11	2010	Treatment with sorafenib enhanced TRAIL-induced Annexin V staining and release of mitochondrial cytochrome c and AIF.	Sorafenib	15-24	cytochrome c, somatic	Homo sapiens	96-108	
21604268-6	2012	However, sorafenib"s main anti-tumor activity seems to occur through cell death induction which correlated with caspase activation, increase in the percentage of hypodiploid cells, activation of BAX and BAK and cytochrome c release from mitochondria to cytosol.	Sorafenib	9-18	cytochrome c, somatic	Homo sapiens	211-223	
20054642-5	2010	At concentrations of 5-10 muM the growth-inhibitory effect of sorafenib was associated with the induction of apoptosis, as indicated by release of cytochrome c and Apoptosis-Inducing Factor into the cytosol, activation of caspase-9 and caspase-7, and PARP-1 cleavage.	Sorafenib	62-71	cytochrome c, somatic	Homo sapiens	147-159	
20473320-5	2010	Sorafenib induced caspase-3 cleavage and the mitochondrial release of cytochrome c.	Sorafenib	0-9	cytochrome c, somatic	Homo sapiens	70-82	
17634558-7	2007	Combined but not individual treatment of CML cells with vorinostat and sorafenib triggered pronounced mitochondrial dysfunction (i.e., cytochrome c, Smac, and AIF release), caspase activation, poly(ADP-ribose) polymerase cleavage, and down-regulation of Mcl-1.	Sorafenib	71-80	cytochrome c, somatic	Homo sapiens	135-147	
16985072-3	2006	Sorafenib and bortezomib synergistically induced a marked increase in mitochondrial injury and apoptosis, reflected by cytochrome c release, caspase-3 cleavage, and poly(ADP-ribose) polymerase degradation in a broad range of solid tumor and leukemia cell lines.	Sorafenib	0-9	cytochrome c, somatic	Homo sapiens	119-131	
16452220-6	2006	BAY 43-9006 induced poly(ADP-ribose) polymerase cleavage and the mitochondrial release of cytochrome c and SMAC.	Sorafenib	0-11	cytochrome c, somatic	Homo sapiens	90-102	
16109713-2	2005	Here we report that treatment with BAY 43-9006 results in marked cytochrome c and AIF release into the cytosol, caspase-9, -8, -7, and -3 activation, and apoptosis in human leukemia cells (U937, Jurkat, and K562).	Sorafenib	35-46	cytochrome c, somatic	Homo sapiens	65-77	
16109713-8	2005	Finally, ectopic expression of Mcl-1 in leukemic cells markedly inhibited BAY 43-9006-mediated cytochrome c cytosolic release, caspase-9, -7, and -3 activation, as well as cell death, indicating that Mcl-1 operates upstream of cytochrome c release and caspase activation.	Sorafenib	74-85	cytochrome c, somatic	Homo sapiens	95-107	
16109713-8	2005	Finally, ectopic expression of Mcl-1 in leukemic cells markedly inhibited BAY 43-9006-mediated cytochrome c cytosolic release, caspase-9, -7, and -3 activation, as well as cell death, indicating that Mcl-1 operates upstream of cytochrome c release and caspase activation.	Sorafenib	74-85	cytochrome c, somatic	Homo sapiens	227-239