PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
13679234-0	2003	A new bisphosphonate, YM529 induces apoptosis in HL60 cells by decreasing phosphorylation of single survival signal ERK.	Diphosphonates	6-20	mitogen-activated protein kinase 1	Homo sapiens	116-119	
20506157-9	2010	Finally, the bisphosphonate ibandronate, that hindered activation of the MEK/ERK pathway significantly inhibited both basal and IL-1beta dependent RANKL expression by cells.	Diphosphonates	13-27	mitogen-activated protein kinase 1	Homo sapiens	77-80	
15590626-7	2005	Connexin 43/ERK-mediated anti-apoptosis induced by bisphosphonates requires the kinase activity of the cytoplasmic target of ERKs, p90(RSK), which in turn phosphorylates the pro-apoptotic protein BAD and C/EBPbeta.	Diphosphonates	51-66	mitogen-activated protein kinase 1	Homo sapiens	12-15	
13679234-12	2003	These results suggest that YM529, the new bisphosphonate, induced apoptosis when inhibit GGPP synthase and consequently decreased the levels of phosphorylated ERK, which is a survival signal; moreover, during this process, there is no influence on NF-kappaB, Akt, p38, and Bcl-2.	Diphosphonates	42-56	mitogen-activated protein kinase 1	Homo sapiens	159-162	
13679234-12	2003	These results suggest that YM529, the new bisphosphonate, induced apoptosis when inhibit GGPP synthase and consequently decreased the levels of phosphorylated ERK, which is a survival signal; moreover, during this process, there is no influence on NF-kappaB, Akt, p38, and Bcl-2.	Diphosphonates	42-56	mitogen-activated protein kinase 1	Homo sapiens	264-267	
11741942-1	2002	Bisphosphonates, drugs used widely in the treatment of bone diseases, prevent osteoblast and osteocyte apoptosis by a mechanism involving extracellular signal-regulated kinase (ERK) activation.	Diphosphonates	0-15	mitogen-activated protein kinase 1	Homo sapiens	138-175	
11741942-1	2002	Bisphosphonates, drugs used widely in the treatment of bone diseases, prevent osteoblast and osteocyte apoptosis by a mechanism involving extracellular signal-regulated kinase (ERK) activation.	Diphosphonates	0-15	mitogen-activated protein kinase 1	Homo sapiens	177-180	
11741942-2	2002	We report herein that hexameric connexin (Cx)-43 hemichannels, but not gap junctions, are the essential transducers of the ERK-activating/anti-apoptotic effects of bisphosphonates.	Diphosphonates	164-179	mitogen-activated protein kinase 1	Homo sapiens	123-126	
25628928-6	2015	In this study, we found that bisphosphonates and statins inhibited MIP-1alpha mRNA and MIP-1alpha secretion and suppressed extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation by inhibiting Ras prenylation.	Diphosphonates	29-44	mitogen-activated protein kinase 1	Homo sapiens	123-164	
25628928-8	2015	These results indicate that bisphosphonates and statins suppress the Ras/mitogen-activated protein kinase kinase/ERK/AML-1A and Ras/phosphatidylinositol-3 kinase/Akt/AML-1A pathways, thereby inhibiting MIP-1alpha secretion by MM cells.	Diphosphonates	28-43	mitogen-activated protein kinase 1	Homo sapiens	113-116	
25628928-0	2015	Bisphosphonates and statins inhibit expression and secretion of MIP-1alpha via suppression of Ras/MEK/ERK/AML-1A and Ras/PI3K/Akt/AML-1A pathways.	Diphosphonates	0-15	mitogen-activated protein kinase 1	Homo sapiens	102-105	
23607938-6	2013	It also activated ERK, sensitized spiral ganglion cells (SGC) to apoptosis, and inhibited proliferation and survival of cochlear stem cells in vitro, which could be rescued by treatment with exogenous OPG, an ERK inhibitor, or bisphosphonate.	Diphosphonates	227-241	mitogen-activated protein kinase 1	Homo sapiens	209-212