PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	72-80	
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	
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	
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	
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