PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32926024-6	2020	Accordingly, the levels of ER stress-related factors (especially, CHOP and GADD34) and of phosphorylated JNK increased upon CuCl2 and ZnCl2 co-treatment, whereas pre-treatment with seleno-l-methionine significantly suppressed these upregulations.	cupric chloride	124-129	mitogen-activated protein kinase 8	Mus musculus	105-108	
30768131-7	2019	Accordingly, we found that phosphorylated (ie, active) forms of SAPK/JNK (p46 and p54) are increased by CuCl2 and ZnCl2 co-treatment in hypothalamic neuronal mouse cells (GT1-7 cells).	cupric chloride	104-109	mitogen-activated protein kinase 8	Mus musculus	69-72	
30768131-8	2019	Downstream factors of SAPK/JNK, phospho-c-Jun, and phospho-activating transcription factor 2 are also induced by CuCl2 and ZnCl2 co-treatment.	cupric chloride	113-118	mitogen-activated protein kinase 8	Mus musculus	27-30	
30768131-9	2019	Moreover, an inhibitor of the SAPK/JNK signaling pathway, SP600125, significantly suppressed neuronal cell death and activation of the SAPK/JNK signaling pathway induced by CuCl2 and ZnCl2 cotreatment.	cupric chloride	173-178	mitogen-activated protein kinase 8	Mus musculus	35-38	
30768131-9	2019	Moreover, an inhibitor of the SAPK/JNK signaling pathway, SP600125, significantly suppressed neuronal cell death and activation of the SAPK/JNK signaling pathway induced by CuCl2 and ZnCl2 cotreatment.	cupric chloride	173-178	mitogen-activated protein kinase 8	Mus musculus	140-143	
30768131-11	2019	On the basis of these results, our findings suggest that activation of ZnCl2-dependent SAPK/JNK signaling pathway is important in neuronal cell death, and CuCl2-induced oxidative stress triggers the activation of this pathway.	cupric chloride	155-160	mitogen-activated protein kinase 8	Mus musculus	92-95