PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29479036-6	2018	Moreover, the combination prolonged the phosphorylation of mitogen-activated protein kinase (MAPK) members, including c-Jun-N-terminal kinase (JNK), p38, and extracellular signal related kinases (ERK), and increased intracellular reactive oxygen species (ROS), in comparison to treatment of NaAsO2 or TNF-alpha alone.	sodium arsenite	291-297	mitogen-activated protein kinase 1	Homo sapiens	93-97	
14962831-3	2004	We demonstrated that inhibition of p38 MAPK with SB-203580 and SB-239063 enhanced H(2)O(2)-stimulated ERK phosphorylation, whereas preactivation of p38 MAPK with sodium arsenite reduced H(2)O(2)-stimulated ERK phosphorylation.	sodium arsenite	162-177	mitogen-activated protein kinase 1	Homo sapiens	35-38	
23219847-11	2013	Sodium arsenite also negatively affects neuronal differentiation of NSC through overactivation of MEK-ERK and suppression of PI3K-AKT.	sodium arsenite	0-15	mitogen-activated protein kinase 1	Homo sapiens	102-105	
14962831-3	2004	We demonstrated that inhibition of p38 MAPK with SB-203580 and SB-239063 enhanced H(2)O(2)-stimulated ERK phosphorylation, whereas preactivation of p38 MAPK with sodium arsenite reduced H(2)O(2)-stimulated ERK phosphorylation.	sodium arsenite	162-177	mitogen-activated protein kinase 1	Homo sapiens	148-151	
32278034-8	2020	When the ERK signaling inhibitor PD98095 was used, there was a similar result that mitophagy was reduced though in contrast with CsA the apoptosis rate was also decreased compared with NaAsO2 alone.	sodium arsenite	185-191	mitogen-activated protein kinase 1	Homo sapiens	9-12	
32278034-9	2020	This result, along with the increased levels of ERK measured here in response to NaAsO2, indicates that ERK activation is a second key molecular response to NaAsO2 through the activation of both apoptosis and mitophagy.	sodium arsenite	81-87	mitogen-activated protein kinase 1	Homo sapiens	48-51	
32278034-9	2020	This result, along with the increased levels of ERK measured here in response to NaAsO2, indicates that ERK activation is a second key molecular response to NaAsO2 through the activation of both apoptosis and mitophagy.	sodium arsenite	81-87	mitogen-activated protein kinase 1	Homo sapiens	104-107	
32278034-9	2020	This result, along with the increased levels of ERK measured here in response to NaAsO2, indicates that ERK activation is a second key molecular response to NaAsO2 through the activation of both apoptosis and mitophagy.	sodium arsenite	157-163	mitogen-activated protein kinase 1	Homo sapiens	48-51	
32278034-9	2020	This result, along with the increased levels of ERK measured here in response to NaAsO2, indicates that ERK activation is a second key molecular response to NaAsO2 through the activation of both apoptosis and mitophagy.	sodium arsenite	157-163	mitogen-activated protein kinase 1	Homo sapiens	104-107	
32278034-11	2020	Mitophagy is increased in response to a secondary effect of NaAsO2 on ERK signaling that activates both mitophagy and apoptosis.	sodium arsenite	60-66	mitogen-activated protein kinase 1	Homo sapiens	70-73	
32278034-13	2020	When ERK signaling is inhibited by PD98095 both the levels of apoptosis and mitophagy are decreased compared with the response produced by NaAsO2 alone in comparison to the inhibition of mitophagy by CsA that reduced mitophagy but dramatically increased apoptosis in response.	sodium arsenite	139-145	mitogen-activated protein kinase 1	Homo sapiens	5-8	
32278034-0	2020	PINK1/Parkin-mediated mitophagy is involved in NaAsO2-induced apoptosis of human hepatic cells through activation of ERK signaling.	sodium arsenite	47-53	mitogen-activated protein kinase 1	Homo sapiens	117-120