PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31639165-8	2019	Glycerol-induced AKI triggered multiple signal mediators of NF-kappaB pathway as well as the elevation of ERK1/2 protein and p38 phosphorylation.	Glycerol	0-8	mitogen-activated protein kinase 1	Homo sapiens	125-128	
26359088-9	2015	Moreover, the increase in glycerol release induced by widdrol was almost completely blocked by PKC, MEK, and ERK inhibitors.	Glycerol	26-34	mitogen-activated protein kinase 1	Homo sapiens	109-112	
26987986-3	2016	Yet, in previous studies we identified mutations in the yeast MAPK high osmolarity glycerol (Hog1) that render it capable of spontaneous autophosphorylation and consequently intrinsically active (MKK-independent).	Glycerol	83-91	mitogen-activated protein kinase 1	Homo sapiens	62-66	
25356552-3	2014	The filamentous growth MAPK pathway shares components with a p38-type High Osmolarity Glycerol response (HOG) pathway, which regulates the response to changes in osmolarity.	Glycerol	86-94	mitogen-activated protein kinase 1	Homo sapiens	23-27	
25356552-3	2014	The filamentous growth MAPK pathway shares components with a p38-type High Osmolarity Glycerol response (HOG) pathway, which regulates the response to changes in osmolarity.	Glycerol	86-94	mitogen-activated protein kinase 1	Homo sapiens	61-64	
16155875-5	2005	In addition, a variety of kinases, including protein kinase A (PKA) and extracellular signal-regulated kinase (ERK) were also phosphorylated as the result of MSH treatment, and their specific inhibitors caused a reduction in MSH-induced glycerol release and HSL activity, indicating that MSH-induced lipolysis was mediated by these kinases.	Glycerol	237-245	mitogen-activated protein kinase 1	Homo sapiens	72-109	
16155875-5	2005	In addition, a variety of kinases, including protein kinase A (PKA) and extracellular signal-regulated kinase (ERK) were also phosphorylated as the result of MSH treatment, and their specific inhibitors caused a reduction in MSH-induced glycerol release and HSL activity, indicating that MSH-induced lipolysis was mediated by these kinases.	Glycerol	237-245	mitogen-activated protein kinase 1	Homo sapiens	111-114	
21701568-6	2011	Moreover, SAA significantly increased porcine adipocyte glycerol release and lipase activity, which was inhibited by either ERK (PD98059) or PKA (H89) inhibitors, suggesting that ERK and PKA were involved in mediating SAA enhanced lipolysis.	Glycerol	56-64	mitogen-activated protein kinase 1	Homo sapiens	124-127