PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29348704-0	2017	Stimulation of Alpha7 Nicotinic Acetylcholine Receptor Attenuates Nicotine-Induced Upregulation of MMP, MCP-1, and RANTES through Modulating ERK1/2/AP-1 Signaling Pathway in RAW264.7 and MOVAS Cells.	Nicotine	66-74	jun proto-oncogene	Mus musculus	148-152	
29348704-7	2017	When cells were pretreated with PNU-282987, nicotine-induced activations of ERK1/2 and c-Jun in RAW264.7 cells and c-Jun in MOVAS cells were effectively inhibited.	Nicotine	44-52	jun proto-oncogene	Mus musculus	87-92	
29348704-9	2017	Treatment with alpha7-nAChR agonist inhibits nicotine-induced upregulation of MMP and inflammatory cytokines through modulating ERK1/2/AP-1 signaling in RAW264.7 cells and AP-1 in MOVAS cells, providing a new therapeutic for abdominal aortic aneurysm.	Nicotine	45-53	jun proto-oncogene	Mus musculus	135-139	
29348704-9	2017	Treatment with alpha7-nAChR agonist inhibits nicotine-induced upregulation of MMP and inflammatory cytokines through modulating ERK1/2/AP-1 signaling in RAW264.7 cells and AP-1 in MOVAS cells, providing a new therapeutic for abdominal aortic aneurysm.	Nicotine	45-53	jun proto-oncogene	Mus musculus	172-176	
29348704-4	2017	Nicotine markedly stimulated the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2) and c-Jun in RAW264.7 cells.	Nicotine	0-8	jun proto-oncogene	Mus musculus	106-111	
29348704-5	2017	Pretreatment with U0126 significantly suppressed phosphorylation of ERK1/2 and further attenuated nicotine-induced activation of c-Jun and upregulation of MMP-2, MMP-9, monocyte chemotactic protein- (MCP-) 1, and regulated upon activation normal T cell expressed and secreted (RANTES).	Nicotine	98-106	jun proto-oncogene	Mus musculus	129-134	
29348704-6	2017	Similarly, nicotine treatment also increased phosphorylation of c-Jun and expressions of MMP-2, MMP-9, MCP-1, and RANTES in MOVAS cells.	Nicotine	11-19	jun proto-oncogene	Mus musculus	64-69	
25430056-6	2015	Both cFos and phosphorylated-cJun (p-cJun) were immediately increased in the nucleus, together with an increase of calmodulin kinase (CaMK) IV but not CaMKII expression after nicotine exposure.	Nicotine	175-183	jun proto-oncogene	Mus musculus	29-33	
25430056-6	2015	Both cFos and phosphorylated-cJun (p-cJun) were immediately increased in the nucleus, together with an increase of calmodulin kinase (CaMK) IV but not CaMKII expression after nicotine exposure.	Nicotine	175-183	jun proto-oncogene	Mus musculus	37-41	
25430056-8	2015	These results indicate that nAChR activation by nicotine upregulates IP3 R-1 via increase of activator protein-1, which is a cFos and cJun dimmer, in the nucleus, with activation of Ca(2+) signaling transduction processes.	Nicotine	48-56	jun proto-oncogene	Mus musculus	134-138