PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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