PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27035858-6	2016	Low cytotoxic doses of DTT transiently activated c-JNU N-terminal kinase (JNK) and p38, whereas high dose of DTT persistently activated JNK and p38 and simultaneously reduced extracellular signal-regulated kinase (ERK) activity.	Dithiothreitol	23-26	mitogen-activated protein kinase 8	Homo sapiens	49-72	
27035858-6	2016	Low cytotoxic doses of DTT transiently activated c-JNU N-terminal kinase (JNK) and p38, whereas high dose of DTT persistently activated JNK and p38 and simultaneously reduced extracellular signal-regulated kinase (ERK) activity.	Dithiothreitol	23-26	mitogen-activated protein kinase 8	Homo sapiens	74-77	
27035858-6	2016	Low cytotoxic doses of DTT transiently activated c-JNU N-terminal kinase (JNK) and p38, whereas high dose of DTT persistently activated JNK and p38 and simultaneously reduced extracellular signal-regulated kinase (ERK) activity.	Dithiothreitol	109-112	mitogen-activated protein kinase 8	Homo sapiens	136-139	
17054907-5	2006	A NO donor S-nitro-N-acetyl-dl-penicillamine (SNAP) inhibited JNK activity in vitro, and this inhibition was reversed by a thiol-reducing agent, dithiothreitol.	Dithiothreitol	145-159	mitogen-activated protein kinase 8	Homo sapiens	62-65	
16124869-6	2006	Analysis of the phosphorylated status of major components in MAPK signalling pathways indicated that thapsigargin and DTT (dithiothreitol) but not tunicamycin could trigger the PERK-dependent activation of JNK (c-Jun N-terminal kinase) and p38 MAPK.	Dithiothreitol	118-121	mitogen-activated protein kinase 8	Homo sapiens	206-209	
16124869-6	2006	Analysis of the phosphorylated status of major components in MAPK signalling pathways indicated that thapsigargin and DTT (dithiothreitol) but not tunicamycin could trigger the PERK-dependent activation of JNK (c-Jun N-terminal kinase) and p38 MAPK.	Dithiothreitol	118-121	mitogen-activated protein kinase 8	Homo sapiens	211-234	
16124869-6	2006	Analysis of the phosphorylated status of major components in MAPK signalling pathways indicated that thapsigargin and DTT (dithiothreitol) but not tunicamycin could trigger the PERK-dependent activation of JNK (c-Jun N-terminal kinase) and p38 MAPK.	Dithiothreitol	123-137	mitogen-activated protein kinase 8	Homo sapiens	206-209	
16124869-6	2006	Analysis of the phosphorylated status of major components in MAPK signalling pathways indicated that thapsigargin and DTT (dithiothreitol) but not tunicamycin could trigger the PERK-dependent activation of JNK (c-Jun N-terminal kinase) and p38 MAPK.	Dithiothreitol	123-137	mitogen-activated protein kinase 8	Homo sapiens	211-234	
12206715-8	2002	In addition, dithiothreitol also suppressed both apoptosis and JNK/p38 activation by EGCG, and EGCG-induced activation of MAP kinase kinase (MKK) 3/6, MKK4 and apoptosis-regulating kinase 1 (ASK1) was suppressed by NAC.	Dithiothreitol	13-27	mitogen-activated protein kinase 8	Homo sapiens	63-66	
10734112-4	2000	Interestingly, pretreatment with the antioxidants, N-acetyl-L-cysteine, dithiothreitol, and glutathione, impaired chelerythrine-induced JNK1 and p38 activation.	Dithiothreitol	72-86	mitogen-activated protein kinase 8	Homo sapiens	136-140	
10644709-6	2000	The in vitro inhibition of JNK/SAPK by selenite was reversed by the addition of reducing agents such as dithiothreitol and beta-mercaptoethanol.	Dithiothreitol	104-118	mitogen-activated protein kinase 8	Homo sapiens	27-30