PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27723793-5	2016	Using inhibitors of cell signaling we have shown that Src family kinases, p38 MAPK, ERK1/2 and GSK3beta are required for the transition between mES and EPL cells.	2-(N-morpholino)ethanesulfonic acid	144-147	mitogen-activated protein kinase 14	Mus musculus	74-82	
22878015-7	2013	Taken together, these results suggest that NO-induced apoptosis in mES cells was mediated through p38 MAP kinase/ERK signaling pathway by triggering caspases activation and Bax translocation from the cytosol to the mitochondria.	2-(N-morpholino)ethanesulfonic acid	67-70	mitogen-activated protein kinase 14	Mus musculus	98-101	
22937108-7	2012	The anti-inflammatory effect of MES+HS was mediated by glomerular activation of c-jun NH(2)-terminal kinase 1/2 (JNK1/2) and p38-dependent pathways ex vivo.	2-(N-morpholino)ethanesulfonic acid	32-35	mitogen-activated protein kinase 14	Mus musculus	125-128	
22937108-8	2012	Collectively, our studies show that combination treatment of MES and HS confers anti-proteinuric and anti-inflammatory effects on Alport mice likely through the activation of multiple signaling pathways including PI3K-Akt, Hsp72, JNK1/2, and p38 pathways, providing a novel candidate therapeutic strategy to decelerate the progression of patho-phenotypes in Alport syndrome.	2-(N-morpholino)ethanesulfonic acid	61-64	mitogen-activated protein kinase 14	Mus musculus	242-245