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