PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10229667-5	1999	The cleavage of Bcl-2 was inhibited by a caspase-3 (CPP32)-specific inhibitor [acetyl-Asp-Glu-Val-Asp-CHO (DEVD-CHO)] but not caspase 1 inhibitor (acetyl-Tyr-Val-Ala-Asp-CHO), suggesting that Bcl-2 is a proteolytic substrate of a caspase-3-like protease activated during apoptosis.	acetyl-aspartyl-glutamyl-valyl-aspartal	79-105	BCL2 apoptosis regulator	Homo sapiens	16-21	
16149076-5	2005	The caspase inhibitor acetyl-Asp-Glu-Val-Asp-aldehyde (Ac-DEVD-CHO) effectively inhibited JNK/SAPK activation, bcl-2 phosphorylation and partially attenuated the ROS production induced by docetaxel.	acetyl-aspartyl-glutamyl-valyl-aspartal	22-53	BCL2 apoptosis regulator	Homo sapiens	111-116	
16149076-5	2005	The caspase inhibitor acetyl-Asp-Glu-Val-Asp-aldehyde (Ac-DEVD-CHO) effectively inhibited JNK/SAPK activation, bcl-2 phosphorylation and partially attenuated the ROS production induced by docetaxel.	acetyl-aspartyl-glutamyl-valyl-aspartal	55-66	BCL2 apoptosis regulator	Homo sapiens	111-116	
11032173-7	2000	The results indicate that activated caspase-3 can promote the movement of intracellular calcium from Golgi"s apparatus to nucleus, and the process is inhibited by Ac-DEVD-CHO (inhibitor of caspase-3), and that Bcl-2 can inhibit the movement and accumulation of intracellular calcium in nucleus through its inhibition on caspase-3.	acetyl-aspartyl-glutamyl-valyl-aspartal	163-174	BCL2 apoptosis regulator	Homo sapiens	210-215	
10229667-5	1999	The cleavage of Bcl-2 was inhibited by a caspase-3 (CPP32)-specific inhibitor [acetyl-Asp-Glu-Val-Asp-CHO (DEVD-CHO)] but not caspase 1 inhibitor (acetyl-Tyr-Val-Ala-Asp-CHO), suggesting that Bcl-2 is a proteolytic substrate of a caspase-3-like protease activated during apoptosis.	acetyl-aspartyl-glutamyl-valyl-aspartal	79-105	BCL2 apoptosis regulator	Homo sapiens	192-197	
9894610-4	1998	Here we report that Bcl-2 and benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), a broad spectrum caspase inhibitor, prevent loss of mitochondrial membrane potential (delta psi m) and the production of reactive oxygen species (ROS) caused by GC, while acetyl-Asp-Glu-Val-Asp-aldehyde (Ac-DEVD-CHO), an inhibitor of the caspase-3 family proteases, does not.	acetyl-aspartyl-glutamyl-valyl-aspartal	267-298	BCL2 apoptosis regulator	Homo sapiens	20-25	
9894610-4	1998	Here we report that Bcl-2 and benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), a broad spectrum caspase inhibitor, prevent loss of mitochondrial membrane potential (delta psi m) and the production of reactive oxygen species (ROS) caused by GC, while acetyl-Asp-Glu-Val-Asp-aldehyde (Ac-DEVD-CHO), an inhibitor of the caspase-3 family proteases, does not.	acetyl-aspartyl-glutamyl-valyl-aspartal	300-311	BCL2 apoptosis regulator	Homo sapiens	20-25	
28082995-4	2016	Total peroxidase activity was lower in Bcl-2 21 treated microspore cultures at 96 h of treatment compared to control and Ac-DEVD-CHO.	acetyl-aspartyl-glutamyl-valyl-aspartal	121-132	BCL2 apoptosis regulator	Homo sapiens	39-44