PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30338935-0	2019	Cardiac-specific Mst1 deficiency inhibits ROS-mediated JNK signalling to alleviate Ang II-induced cardiomyocyte apoptosis.	Reactive Oxygen Species	42-45	mitogen-activated protein kinase 8	Homo sapiens	55-58	
30338935-5	2019	In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling.	Reactive Oxygen Species	191-194	mitogen-activated protein kinase 8	Homo sapiens	263-286	
30338935-5	2019	In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling.	Reactive Oxygen Species	191-194	mitogen-activated protein kinase 8	Homo sapiens	288-291	
30338935-7	2019	Thus, cardiac-specific Mst1 knockout inhibits ROS-mediated JNK signalling to block Ang II-induced cardiomyocyte apoptosis, suggesting Mst1 as a potential therapeutic target for treatment of RAAS-activated heart failure.	Reactive Oxygen Species	46-49	mitogen-activated protein kinase 8	Homo sapiens	59-62