PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Methyl Methanesulfonate 281-284 mitogen-activated protein kinase 8 Homo sapiens 72-80 12663670-3 2003 We have observed that four DNA-damaging agents (cisplatin, actinomycin D, MMS, and etoposide), but not the cisplatin isomer, transplatin, which does not readily damage DNA, strongly activate JNK, p38, and extracellular signal-regulated kinase (ERK), and strongly increase phosphorylation and ATF2-dependent transcriptional activity. Methyl Methanesulfonate 74-77 mitogen-activated protein kinase 8 Homo sapiens 191-194 11494044-7 2001 In vitro phosphorylation assay, carried out with the immunoprecipates of MMS-treated cells, showed an increased phosphorylation of p53 by c-Jun kinase 1 (JNK1) at early time points (2.5 h). Methyl Methanesulfonate 73-76 mitogen-activated protein kinase 8 Homo sapiens 138-152 11494044-7 2001 In vitro phosphorylation assay, carried out with the immunoprecipates of MMS-treated cells, showed an increased phosphorylation of p53 by c-Jun kinase 1 (JNK1) at early time points (2.5 h). Methyl Methanesulfonate 73-76 mitogen-activated protein kinase 8 Homo sapiens 154-158 11429782-1 2001 The alkylating agent methylmethanesulfonate (MMS) activates the c-jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and the p38 mitogen-activated protein kinase (p38MAPK) pathways via different mechanisms of action. Methyl Methanesulfonate 21-43 mitogen-activated protein kinase 8 Homo sapiens 64-87 11429782-1 2001 The alkylating agent methylmethanesulfonate (MMS) activates the c-jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and the p38 mitogen-activated protein kinase (p38MAPK) pathways via different mechanisms of action. Methyl Methanesulfonate 21-43 mitogen-activated protein kinase 8 Homo sapiens 89-92 11429782-1 2001 The alkylating agent methylmethanesulfonate (MMS) activates the c-jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and the p38 mitogen-activated protein kinase (p38MAPK) pathways via different mechanisms of action. Methyl Methanesulfonate 45-48 mitogen-activated protein kinase 8 Homo sapiens 64-87 11429782-1 2001 The alkylating agent methylmethanesulfonate (MMS) activates the c-jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and the p38 mitogen-activated protein kinase (p38MAPK) pathways via different mechanisms of action. Methyl Methanesulfonate 45-48 mitogen-activated protein kinase 8 Homo sapiens 89-92 11429782-3 2001 The way in which MMS can activate JNK/SAPK has not been elucidated. Methyl Methanesulfonate 17-20 mitogen-activated protein kinase 8 Homo sapiens 34-42 11429782-9 2001 Our results suggest that activation of JNK/SAPKs by MMS may involve the induction of MIG-6. Methyl Methanesulfonate 52-55 mitogen-activated protein kinase 8 Homo sapiens 39-42 10085098-3 1999 Here we demonstrate that methylmethane sulfonate (MMS)-induced activation of JNK is inhibited by overexpression of the anti-apoptotic protein Bcl-xL, but not by caspase inhibitors CrmA and p35. Methyl Methanesulfonate 25-48 mitogen-activated protein kinase 8 Homo sapiens 77-80 10085098-3 1999 Here we demonstrate that methylmethane sulfonate (MMS)-induced activation of JNK is inhibited by overexpression of the anti-apoptotic protein Bcl-xL, but not by caspase inhibitors CrmA and p35. Methyl Methanesulfonate 50-53 mitogen-activated protein kinase 8 Homo sapiens 77-80 10085098-8 1999 Hence, treatment of Bcl-xL cells with sodium vanadate, a tyrosine phosphatase inhibitor, restores MMS-induced activation of RAFTK and JNK. Methyl Methanesulfonate 98-101 mitogen-activated protein kinase 8 Homo sapiens 134-137 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Methyl Methanesulfonate 95-98 mitogen-activated protein kinase 8 Homo sapiens 72-80 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Methyl Methanesulfonate 95-98 mitogen-activated protein kinase 8 Homo sapiens 72-75 28542436-5 2017 Phosphoproteomic and site-directed mutagenesis analyses of lamin B1 isolated from control and MMS-treated nuclei identified T575 as a JNK site phosphorylated after stress. Methyl Methanesulfonate 94-97 mitogen-activated protein kinase 8 Homo sapiens 134-137 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Methyl Methanesulfonate 281-284 mitogen-activated protein kinase 8 Homo sapiens 72-75 7721728-7 1995 JNK is shown to be activated by UVC and MMS treatment, while MAP kinase activation occurs only with UVC. Methyl Methanesulfonate 40-43 mitogen-activated protein kinase 8 Homo sapiens 0-3