PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28978109-6	2017	Sorafenib significantly reduces Second mitochondria-derived activator of caspases (Smac) mimetic-induced necroptosis in apoptosis-resistant acute myeloid leukemia (AML) cells as well as Smac mimetic/Tumor Necrosis Factor (TNF)alpha-induced necroptosis in FADD-deficient acute lymphoblastic leukemia (ALL) cells.	Sorafenib	0-9	diablo IAP-binding mitochondrial protein	Homo sapiens	83-87	
28978109-8	2017	Furthermore, Sorafenib blocks Smac mimetic-mediated phosphorylation of mixed-lineage kinase domain-like protein (MLKL) that marks its activation, indicating that Sorafenib targets components upstream of MLKL such as RIP1 and RIP3.	Sorafenib	13-22	diablo IAP-binding mitochondrial protein	Homo sapiens	30-34	
28978109-8	2017	Furthermore, Sorafenib blocks Smac mimetic-mediated phosphorylation of mixed-lineage kinase domain-like protein (MLKL) that marks its activation, indicating that Sorafenib targets components upstream of MLKL such as RIP1 and RIP3.	Sorafenib	162-171	diablo IAP-binding mitochondrial protein	Homo sapiens	30-34	
28978109-9	2017	Intriguingly, Sorafenib reduces the Smac mimetic/TNFalpha-stimulated interaction of RIP1 with RIP3 and MLKL, demonstrating that it interferes with the assembly of the necrosome complex.	Sorafenib	14-23	diablo IAP-binding mitochondrial protein	Homo sapiens	36-40	
28978109-10	2017	Importantly, Sorafenib significantly protects primary, patient-derived AML blasts from Smac mimetic-induced necroptosis.	Sorafenib	13-22	diablo IAP-binding mitochondrial protein	Homo sapiens	87-91	
17991738-4	2008	Pharmacologic inhibition and/or down-modulation of the kinase enhances sorafenib-induced apoptosis as determined by propidium iodide staining and by assessing the mitochondrial release of apoptosis-inducing factor and Smac/DIABLO.	Sorafenib	71-80	diablo IAP-binding mitochondrial protein	Homo sapiens	218-222	
17991738-4	2008	Pharmacologic inhibition and/or down-modulation of the kinase enhances sorafenib-induced apoptosis as determined by propidium iodide staining and by assessing the mitochondrial release of apoptosis-inducing factor and Smac/DIABLO.	Sorafenib	71-80	diablo IAP-binding mitochondrial protein	Homo sapiens	223-229	
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	diablo IAP-binding mitochondrial protein	Homo sapiens	104-108	
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	diablo IAP-binding mitochondrial protein	Homo sapiens	149-153