PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30206205-7	2018	TNFR2/ZVAD-induced production of IL-6 and IL-1beta was largely blocked in necroptosis-resistant MLKL- and RIPK3-deficient macrophages, whereas induction of A20 and TRAF1 remained unaffected.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	6-10	receptor interacting serine/threonine kinase 3	Homo sapiens	106-111	
31416203-6	2019	GTN and z-VAD-fmk induced human breast cancer MDA-MB-231 cells to undergo necroptosis via endoplasmic reticulum (ER) and oxidative stresses, with increased expressions of necroptotic genes such as rip1, rip3, and mlkl.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	8-17	receptor interacting serine/threonine kinase 3	Homo sapiens	203-207	
29286079-9	2018	By contrast, pre-treatment with Z-VAD-FMK, a pan -caspase inhibitor, promoted the increased expression of RIP3 by HG.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	32-41	receptor interacting serine/threonine kinase 3	Homo sapiens	106-110	
28716527-7	2017	Importantly, genetic silencing of key components of necroptosis signaling such as MLKL or RIP3 significantly protects DG-75 cells from BV6/Bortezomib-induced cell death in the presence and even the absence of zVAD.fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	209-213	receptor interacting serine/threonine kinase 3	Homo sapiens	90-94	
28810529-7	2017	SM in presence of zVAD and 3-MA significantly decreased viability and proliferation of HT-29 cells, and expression of RIPK1 and RIPK3 in compare to absence the inhibitors.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	18-22	receptor interacting serine/threonine kinase 3	Homo sapiens	128-133	
26944210-6	2016	Indeed, genetic silencing of key components of necroptosis such as Receptor-Interacting Protein (RIP)3 or mixed lineage kinase domain-like (MLKL) in parallel with administration of zVAD.fmk provides a significantly better protection against BV6/5AC-induced cell death compared to the use of zVAD.fmk alone.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	291-295	receptor interacting serine/threonine kinase 3	Homo sapiens	67-102	
27456663-9	2017	However, in the zVAD pretreated cells, necroptotic cell death with a significant increase in expression of RIP1, RIP3, and MLKL genes was observed Conclusion: The novel hybrid benzoxazole-coumarins effectively induce Caspase-3 dependent apoptosis in HN-5 cancer cells, but also could circumvent the blockage of apoptotic cell death by induction of necroptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	16-20	receptor interacting serine/threonine kinase 3	Homo sapiens	113-117	
29156831-7	2017	Under the stimulation of TNF-alpha and Z-VAD-fmk, the morphologic damage in the Caco-2 cells was aggravated, the proportion of necrosis was increased, and the level of p-RIPK3 and p-MLKL were increased, confirming that the regulated cell death was necroptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	39-48	receptor interacting serine/threonine kinase 3	Homo sapiens	170-175	
27752362-8	2016	Regarding the inhibitors, z-VAD-fmk diminishes the cleaved caspase 8, RIP1, RIP3, and MLKL induced by Tan IIA, and reconstructs the ripoptosome complex, which marks cells moving from apoptosis to necroptosis.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	26-35	receptor interacting serine/threonine kinase 3	Homo sapiens	76-80	
22057483-7	2011	In addition, RIP3-U2OS cell death was decreased by a zVAD-fmk pre-treatment.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	53-61	receptor interacting serine/threonine kinase 3	Homo sapiens	13-17	
17644308-3	2007	In this study, we show that RIP3 is cleaved at Asp328 by caspase-8 under apoptotic stimuli, which is blocked by pan-caspase inhibitor Z-VAD-FMK.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	134-143	receptor interacting serine/threonine kinase 3	Homo sapiens	28-32