PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33276105-4 2021 We found that U87MG and GBM5 cells express similar nAChR subtypes, and choline and nicotine increase their proliferation rate and activate the anti-apoptotic AKT and pro-proliferative ERK pathways. Nicotine 83-91 mitogen-activated protein kinase 1 Homo sapiens 184-187 34230140-8 2021 Western blot and inhibitor assays showed that the nicotine-induced signaling was mediated through MAPK/ERK and AKT signaling pathways in EBV-infected and LMP1-transfected breast cancer cells, respectively. Nicotine 50-58 mitogen-activated protein kinase 1 Homo sapiens 103-106 33355840-8 2021 In addition, we showed that E-cigarettes vapor with and without nicotine induce MUC5AC expression via activation of MAPK (ERK 1/2 and p38) and NF-kappaB signaling pathways in human airway epithelial cells. Nicotine 64-72 mitogen-activated protein kinase 1 Homo sapiens 134-137 32024069-6 2020 Nicotine induced secretion of interleukin 8 (IL-8) by tumor-associated stroma cells in an extracellular signal-regulated kinase (ERK)-dependent fashion. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 90-127 32649943-5 2020 Exposure to nicotine for 96 h led to a significant reduction in the amounts of activated extracellular signal-regulated kinase (ERK) and activated p38 mitogen-activated protein kinases (MAPKs) in SKOV3 cells, and in activated ERK in TOV112D cells. Nicotine 12-20 mitogen-activated protein kinase 1 Homo sapiens 89-126 32649943-5 2020 Exposure to nicotine for 96 h led to a significant reduction in the amounts of activated extracellular signal-regulated kinase (ERK) and activated p38 mitogen-activated protein kinases (MAPKs) in SKOV3 cells, and in activated ERK in TOV112D cells. Nicotine 12-20 mitogen-activated protein kinase 1 Homo sapiens 128-131 32649943-5 2020 Exposure to nicotine for 96 h led to a significant reduction in the amounts of activated extracellular signal-regulated kinase (ERK) and activated p38 mitogen-activated protein kinases (MAPKs) in SKOV3 cells, and in activated ERK in TOV112D cells. Nicotine 12-20 mitogen-activated protein kinase 1 Homo sapiens 226-229 32024069-6 2020 Nicotine induced secretion of interleukin 8 (IL-8) by tumor-associated stroma cells in an extracellular signal-regulated kinase (ERK)-dependent fashion. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 129-132 26530054-0 2016 Nicotine enhances invasion and metastasis of human colorectal cancer cells through the nicotinic acetylcholine receptor downstream p38 MAPK signaling pathway. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 131-134 30912145-8 2019 Moreover, alpha7-nAChR knockdown could only decrease the inhibitory effects of nicotine and PNU-282987 on the phosphorylated extracellular signal-regulated kinase (ERK), not c-Jun amino-terminal kinase and p38. Nicotine 79-87 mitogen-activated protein kinase 1 Homo sapiens 125-162 30912145-8 2019 Moreover, alpha7-nAChR knockdown could only decrease the inhibitory effects of nicotine and PNU-282987 on the phosphorylated extracellular signal-regulated kinase (ERK), not c-Jun amino-terminal kinase and p38. Nicotine 79-87 mitogen-activated protein kinase 1 Homo sapiens 164-167 30912145-8 2019 Moreover, alpha7-nAChR knockdown could only decrease the inhibitory effects of nicotine and PNU-282987 on the phosphorylated extracellular signal-regulated kinase (ERK), not c-Jun amino-terminal kinase and p38. Nicotine 79-87 mitogen-activated protein kinase 1 Homo sapiens 206-209 29338098-0 2018 Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin through inhibition of ERK phosphorylation. Nicotine 70-78 mitogen-activated protein kinase 1 Homo sapiens 127-130 29338098-1 2018 Through activation of the ERK pathway, nicotine, in both normal MCF-10A and low-malignant breast cancer cells (MCF7), promotes increased motility and invasiveness. Nicotine 39-47 mitogen-activated protein kinase 1 Homo sapiens 26-29 27028622-8 2016 Nicotine treatment reduced cell viability dose dependently, increased ROS levels, and increased extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK expression. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 96-133 27028622-8 2016 Nicotine treatment reduced cell viability dose dependently, increased ROS levels, and increased extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK expression. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 135-138 27028622-9 2016 Nicotine increased NF-kappaB activation, which was attenuated by N-acetyl-L-cysteine, and ERK and JNK inhibitors, but was not affected by a p38 MAPK inhibitor. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 90-93 26530054-9 2016 Nicotine increased phosphorylation of p38, ERK, Akt and PI3K p85 but had no effect on phosphorylation of JNK, or NF-kappaB. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 43-46 26530054-11 2016 We concluded that nicotine stimulates the invasion and metastasis of colon cancer cells in vitro via activation of the nAchRs and the p38 MAPK downstream signaling pathway. Nicotine 18-26 mitogen-activated protein kinase 1 Homo sapiens 134-137 29338098-4 2018 This finding suggests that melatonin hampers ERK phosphorylation presumably by targeting a still unknown intermediate factor that connects nicotine stimulation to ERK phosphorylation. Nicotine 139-147 mitogen-activated protein kinase 1 Homo sapiens 45-48 29338098-4 2018 This finding suggests that melatonin hampers ERK phosphorylation presumably by targeting a still unknown intermediate factor that connects nicotine stimulation to ERK phosphorylation. Nicotine 139-147 mitogen-activated protein kinase 1 Homo sapiens 163-166 29039603-0 2017 Blockade of alpha7 nicotinic acetylcholine receptors inhibit nicotine-induced tumor growth and vimentin expression in non-small cell lung cancer through MEK/ERK signaling way. Nicotine 61-69 mitogen-activated protein kinase 1 Homo sapiens 157-160 29039603-8 2017 Furthermore, under the stimulation of nicotine, the MEK/ERK signaling pathway was found to be inhibited when cells were treated with an antagonist of alpha7nAChR or an inhibitor of MEK. Nicotine 38-46 mitogen-activated protein kinase 1 Homo sapiens 56-59 27907022-13 2016 Nicotine enhanced podocyte phosphorylation of ERK1/2, JNK, and p38, and their specific inhibitors attenuated nicotine-induced apoptosis. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 63-66 27907022-13 2016 Nicotine enhanced podocyte phosphorylation of ERK1/2, JNK, and p38, and their specific inhibitors attenuated nicotine-induced apoptosis. Nicotine 109-117 mitogen-activated protein kinase 1 Homo sapiens 63-66 26530054-9 2016 Nicotine increased phosphorylation of p38, ERK, Akt and PI3K p85 but had no effect on phosphorylation of JNK, or NF-kappaB. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 38-41 25565665-7 2015 HIF-2alpha inhibitor and HIF-2alpha siRNA inhibited the effects of nicotine and LPS on the activation of Akt, JAK2 and STAT3, ERK and JNK MAPK, nuclear factor-kappaB, c-Jun, and c-Fos. Nicotine 67-75 mitogen-activated protein kinase 1 Homo sapiens 126-129 25393899-10 2015 Furthermore, pretreatment with isoproterenol or resistin-specific siRNA blocked nicotine plus LPS-induced activation of phosphoinositide-3-kinase, glycogen synthase kinase-3 beta, beta-catenin, p38, ERK, JNK and nuclear factor-kappaB. Nicotine 80-88 mitogen-activated protein kinase 1 Homo sapiens 199-202 25565665-7 2015 HIF-2alpha inhibitor and HIF-2alpha siRNA inhibited the effects of nicotine and LPS on the activation of Akt, JAK2 and STAT3, ERK and JNK MAPK, nuclear factor-kappaB, c-Jun, and c-Fos. Nicotine 67-75 mitogen-activated protein kinase 1 Homo sapiens 138-142 24481039-0 2014 Nicotine exerts neuroprotective effects against beta-amyloid-induced neurotoxicity in SH-SY5Y cells through the Erk1/2-p38-JNK-dependent signaling pathway. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 119-122 26150803-10 2015 Thus, these findings indicate that the direct injection of Tat at the VTA may mediate CREB and ERK activity in response to nicotine-induced locomotor activity. Nicotine 123-131 mitogen-activated protein kinase 1 Homo sapiens 95-98 24481039-3 2014 The aim of the present study was to assess the neuroprotective effects of nicotine against toxicity induced by beta-amyloid (Abeta) in relation to cell apoptosis, and to elucidate the role of the activation of the Erk1/2-p38-JNK pathway and the modulation of anti-apoptotic proteins in the nicotine-induced neuroprotective effects. Nicotine 74-82 mitogen-activated protein kinase 1 Homo sapiens 221-224 25815723-5 2015 In the present study, we show that nicotine can activate the MAPK/ERK/EGR-1 signaling pathway partially through alpha7 nAChR. Nicotine 35-43 mitogen-activated protein kinase 1 Homo sapiens 66-69 23543412-7 2013 Challenge with nicotine triggered phosphorylation of the extracellular signal-regulated kinase (ERK) and the thymoma viral proto-oncogene (Akt), followed by activation of the mammalian target of rapamycin complex 1 (mTORC1)-dependent p70 ribosomal S6 protein kinase. Nicotine 15-23 mitogen-activated protein kinase 1 Homo sapiens 57-94 23199342-8 2013 Resveratrol and Ad-SIRT1 inhibited nicotine and LPS-mediated protein kinase C (PKC), phosphatidylinositol 3-kinase (PI3K), p38, ERK, JNK, MAPK and nuclear factor-kappa B (NF-kappaB) activation. Nicotine 35-43 mitogen-activated protein kinase 1 Homo sapiens 128-131 24481039-9 2014 The phosphorylation of Erk1/2, p38 and JNK increased following treatment with nicotine in the SH-SY5Y cells, whereas caspase-3 activation was inhibited by treatment with nicotine prior to exposure to Abeta25-35. Nicotine 78-86 mitogen-activated protein kinase 1 Homo sapiens 31-34 24481039-10 2014 Of note, these effects of nicotine against Abeta25-35-induced damage were abolished by inhibitors of Erk1/2, p38 and JNK phosphorylation. Nicotine 26-34 mitogen-activated protein kinase 1 Homo sapiens 109-112 24399025-10 2014 The results presented here indicate that nicotine could achieve alpha7 nAChR-mediated proliferation and anti-apoptotic effects by activating Erk-JNK and PI3K-Akt pathways respectively, providing potential therapeutic molecules to deal with smoking-associated human diseases. Nicotine 41-49 mitogen-activated protein kinase 1 Homo sapiens 141-144 24201001-8 2014 Phosphorylation and expression of p38 were increased 1.7- and 1.6-fold, respectively, by nicotine alone, and 1.9- and 2.1-fold by the combined treatment. Nicotine 89-97 mitogen-activated protein kinase 1 Homo sapiens 34-37 24201001-9 2014 Some increase (1.8-fold) was also seen in the phosphorylation of ERK2 at 48 h, in cells exposed to both ethanol and nicotine. Nicotine 116-124 mitogen-activated protein kinase 1 Homo sapiens 65-69 24095863-8 2013 Moreover, P-ERK/ERK ratio was modified by nicotine addition to 5-FU and CPT treated cells in an opposite manner. Nicotine 42-50 mitogen-activated protein kinase 1 Homo sapiens 12-15 24095863-12 2013 Nicotine anti-apoptotic effects were exerted through ERK and AKT pathway activation. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 53-56 23543412-7 2013 Challenge with nicotine triggered phosphorylation of the extracellular signal-regulated kinase (ERK) and the thymoma viral proto-oncogene (Akt), followed by activation of the mammalian target of rapamycin complex 1 (mTORC1)-dependent p70 ribosomal S6 protein kinase. Nicotine 15-23 mitogen-activated protein kinase 1 Homo sapiens 96-99 22614999-7 2013 Nicotine increased phosphorylation of EGFR(tyr992), AKT(ser473), and ERK. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 69-72 23192567-5 2013 NaHS blocked nicotine and LPS-induced activation of p38, ERK, MKP-1, PI3K, PKC, and PKC isoenzymes, and NF-kappaB. Nicotine 13-21 mitogen-activated protein kinase 1 Homo sapiens 57-60 22614999-9 2013 It was therefore concluded that nicotine stimulates the malignant behavior of glioma cells in vitro by activation of the EGFR and downstream AKT and ERK pathways. Nicotine 32-40 mitogen-activated protein kinase 1 Homo sapiens 149-152 21070506-1 2012 From studies in cultured cells and animal models, nicotine and alcohol are known to regulate extracellular signal-regulated kinase 1 and 2 (ERK1/2). Nicotine 50-58 mitogen-activated protein kinase 1 Homo sapiens 93-138 23149874-9 2012 These demonstrate that nicotine has ability to induce CRP expression in macrophages through nAChR-ERK1/2/p38 MAPK-NF-kappaB signal pathway, which contributes to better understanding of the pro-inflammatory and pro-atherosclerotic effects of nicotine in cigarette smokers. Nicotine 23-31 mitogen-activated protein kinase 1 Homo sapiens 105-108 22791813-8 2012 The resulting increase in catecholamine production was associated with significant inductions in the phosphorylation of signaling proteins ERK, CREB, Src and AKT, upregulated protein expression of nAChR subunits alpha3, alpha4, alpha5 and alpha7 and increased responsiveness to nicotine in 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide and cell migration assays. Nicotine 278-286 mitogen-activated protein kinase 1 Homo sapiens 139-142 22188668-8 2012 The nicotinic agonists acetylcholine, nicotine, and its nitrosated carcinogenic derivative NNK induced the phosphorylation of CREB, ERK, Src, and AKT and these responses were inhibited by propranolol. Nicotine 38-46 mitogen-activated protein kinase 1 Homo sapiens 132-135 19804648-2 2009 In this study we sought to characterize the cellular localization of phosphorylated, active ERK in organotypic hippocampal cultures after acute exposure to either Abeta (1-42) or nicotine. Nicotine 179-187 mitogen-activated protein kinase 1 Homo sapiens 92-95 22952803-0 2012 Nicotine promotes proliferation of human nasopharyngeal carcinoma cells by regulating alpha7AChR, ERK, HIF-1alpha and VEGF/PEDF signaling. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 98-101 22952803-4 2012 The mechanism studies showed that the observed stimulation of proliferation was accompanied by the nicotine-mediated simultaneous modulation of alpha7AChR, HIF-1alpha, ERK and VEGF/PEDF signaling. Nicotine 99-107 mitogen-activated protein kinase 1 Homo sapiens 168-171 22952803-7 2012 Nicotine also promoted the phosphorylation of ERK1/2 but not JNK and p38 proteins, thereby induced the activation of ERK/MAPK signaling pathway. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 46-49 22952803-8 2012 Pretreatment with an ERK-selective inhibitor effectively reduced the nicotine-induced proliferation of NPC cells. Nicotine 69-77 mitogen-activated protein kinase 1 Homo sapiens 21-24 22952803-10 2012 Pretreatment with a alpha7AChR or ERK-selective inhibitor or transfection with a HIF-1alpha-specific siRNA in NPC cells significantly inhibited the nicotine-induced HIF-1alpha expression and VEGF/PEDF ratio. Nicotine 148-156 mitogen-activated protein kinase 1 Homo sapiens 34-37 22952803-11 2012 These results therefore indicate that nicotine promotes proliferation of human NPC cells in vitro through simultaneous modulation of alpha7AChR, HIF-1alpha, ERK and VEGF/PEDF signaling and suggest that the related molecules such as HIF-1alpha might be the potential therapeutic targets for tobacco-associated diseases such as nasopharyngeal carcinomas. Nicotine 38-46 mitogen-activated protein kinase 1 Homo sapiens 157-160 21262190-5 2011 Estradiol-BSA administration was associated with 30% decreased nicotine-induced apoptosis and also attenuated nicotine-activated phosphorylation of p38 and ERK. Nicotine 110-118 mitogen-activated protein kinase 1 Homo sapiens 156-159 21262190-10 2011 Clinically, the nicotine in cigarettes might contribute to endothelial dysfunction, whereas ambient estradiol may provide cellular protection against nicotine-induced injury through its functional membrane receptor via MAPK pathway downregulation. Nicotine 150-158 mitogen-activated protein kinase 1 Homo sapiens 219-223 20050989-11 2010 Based on these findings, melatonin is able to minimize the negative effects of nicotine by blocking the activation of ERK and the other signalling pathways in which this enzyme is involved. Nicotine 79-87 mitogen-activated protein kinase 1 Homo sapiens 118-121 19804648-3 2009 RESULTS: We observed that Abeta and nicotine increased the levels of active ERK in distinct cellular localizations. Nicotine 36-44 mitogen-activated protein kinase 1 Homo sapiens 76-79 19804648-4 2009 We also examined whether phospho-ERK was regulated by redox signaling mechanisms and found that increases in active ERK induced by Abeta and nicotine were blocked by inhibitors of NADPH oxidase. Nicotine 141-149 mitogen-activated protein kinase 1 Homo sapiens 33-36 19804648-4 2009 We also examined whether phospho-ERK was regulated by redox signaling mechanisms and found that increases in active ERK induced by Abeta and nicotine were blocked by inhibitors of NADPH oxidase. Nicotine 141-149 mitogen-activated protein kinase 1 Homo sapiens 116-119 17003101-2 2007 In the present study, we further investigated whether beta-adrenoceptors, protein kinase C (PKC), and extracellular signal-regulated kinase-1/2 (ERK1/2) were involved in the modulation of COX-2 expression and cell proliferation by nicotine in AGS, a human gastric adenocarcinoma cell line. Nicotine 231-239 mitogen-activated protein kinase 1 Homo sapiens 102-143 18805435-6 2008 Moreover, in contrast to the dependence of growth promoting effect of nicotine on Erk activation, inhibitor of p38 mitogen-activated protein kinase (MAPK) repressed NNK-induced COX-2 upregulation and resulted in suppression of cell growth. Nicotine 70-78 mitogen-activated protein kinase 1 Homo sapiens 82-85 18448488-6 2008 We found that nicotine simultaneously activates Stat3 and extracellular signal regulated kinase 1/2 (ERK1/2) in T24 cells. Nicotine 14-22 mitogen-activated protein kinase 1 Homo sapiens 58-99 18041576-3 2008 Here, we review previous literatures that focus on the effects of exposure to cocaine, amphetamine, Delta(9)-tetrahydrocannabinol (THC), nicotine, morphine, and alcohol on ERK signaling in the mesocorticolimbic dopamine system; these alterations of ERK signaling have been thought to contribute to the drug"s rewarding effects and to the long-term maladaptation induced by drug abuse. Nicotine 137-145 mitogen-activated protein kinase 1 Homo sapiens 172-175 18041576-3 2008 Here, we review previous literatures that focus on the effects of exposure to cocaine, amphetamine, Delta(9)-tetrahydrocannabinol (THC), nicotine, morphine, and alcohol on ERK signaling in the mesocorticolimbic dopamine system; these alterations of ERK signaling have been thought to contribute to the drug"s rewarding effects and to the long-term maladaptation induced by drug abuse. Nicotine 137-145 mitogen-activated protein kinase 1 Homo sapiens 249-252 17600315-9 2007 The fibronectin-inducing effects of nicotine were associated with activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3-K)/mammalian target of rapamycin (mTOR) signaling pathways, and were abrogated by inhibitors of ERK (PD98059), PI3-K (LY294002), and mTOR (rapamycin), but not by inhibitors of protein kinase (PK)C (calphostin C) and PKA (H89). Nicotine 36-44 mitogen-activated protein kinase 1 Homo sapiens 80-117 17600315-9 2007 The fibronectin-inducing effects of nicotine were associated with activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3-K)/mammalian target of rapamycin (mTOR) signaling pathways, and were abrogated by inhibitors of ERK (PD98059), PI3-K (LY294002), and mTOR (rapamycin), but not by inhibitors of protein kinase (PK)C (calphostin C) and PKA (H89). Nicotine 36-44 mitogen-activated protein kinase 1 Homo sapiens 119-122 17600315-9 2007 The fibronectin-inducing effects of nicotine were associated with activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3-K)/mammalian target of rapamycin (mTOR) signaling pathways, and were abrogated by inhibitors of ERK (PD98059), PI3-K (LY294002), and mTOR (rapamycin), but not by inhibitors of protein kinase (PK)C (calphostin C) and PKA (H89). Nicotine 36-44 mitogen-activated protein kinase 1 Homo sapiens 255-258 16257255-6 2006 Therefore, we concluded that: (i) nicotine obviously up-regulates VCAM-1 and E-selectin expression at 15 min in HUVECs, (ii) nicotine activates HUVECs triggered by the ERK1/2 and p38 phosphorylation with an involvement of intracellular calcium mobilization chiefly mediated by alpha7 nicotinic receptor, (iii) intracellular Ca2+ activates a sequential pathway from alpha7 nicotinic receptor to the phosphorylation of ERK1/2, p38. Nicotine 34-42 mitogen-activated protein kinase 1 Homo sapiens 179-182 16644474-6 2006 Moreover, calcium chelator BAPTA, ERK1/2 inhibitor PD98059, p38 inhibitor SB203580 significantly reduced the production of nicotine-activated surface/soluble VCAM-1 and E-selectin and both of the remained levels were no longer regulated by estrogen. Nicotine 123-131 mitogen-activated protein kinase 1 Homo sapiens 60-63 16644474-7 2006 Our study here provides the information of decrease effect of mER-mediated estrogen through Ca2+ and ERK1/2, p38 MAPK signaling pathway on nicotine-stimulated expression of surface/soluble VCAM-1 and E-selectin in HUVECs. Nicotine 139-147 mitogen-activated protein kinase 1 Homo sapiens 109-112 16257255-6 2006 Therefore, we concluded that: (i) nicotine obviously up-regulates VCAM-1 and E-selectin expression at 15 min in HUVECs, (ii) nicotine activates HUVECs triggered by the ERK1/2 and p38 phosphorylation with an involvement of intracellular calcium mobilization chiefly mediated by alpha7 nicotinic receptor, (iii) intracellular Ca2+ activates a sequential pathway from alpha7 nicotinic receptor to the phosphorylation of ERK1/2, p38. Nicotine 34-42 mitogen-activated protein kinase 1 Homo sapiens 425-428 16257255-6 2006 Therefore, we concluded that: (i) nicotine obviously up-regulates VCAM-1 and E-selectin expression at 15 min in HUVECs, (ii) nicotine activates HUVECs triggered by the ERK1/2 and p38 phosphorylation with an involvement of intracellular calcium mobilization chiefly mediated by alpha7 nicotinic receptor, (iii) intracellular Ca2+ activates a sequential pathway from alpha7 nicotinic receptor to the phosphorylation of ERK1/2, p38. Nicotine 125-133 mitogen-activated protein kinase 1 Homo sapiens 179-182 16257255-6 2006 Therefore, we concluded that: (i) nicotine obviously up-regulates VCAM-1 and E-selectin expression at 15 min in HUVECs, (ii) nicotine activates HUVECs triggered by the ERK1/2 and p38 phosphorylation with an involvement of intracellular calcium mobilization chiefly mediated by alpha7 nicotinic receptor, (iii) intracellular Ca2+ activates a sequential pathway from alpha7 nicotinic receptor to the phosphorylation of ERK1/2, p38. Nicotine 125-133 mitogen-activated protein kinase 1 Homo sapiens 425-428 15813854-7 2005 In addition, nicotine treatment stimulated rapid phosphorylation of Erk1/2 and p-38 in endothelial cells. Nicotine 13-21 mitogen-activated protein kinase 1 Homo sapiens 79-83 15733153-8 2005 A nicotine concentration of 5 mm was found to induce extracellular signal-regulated kinase (ERK) phosphorylation in a time-dependent manner (p<0.05). Nicotine 2-10 mitogen-activated protein kinase 1 Homo sapiens 53-90 12421819-6 2003 Nicotine induces activation of PKC alpha and the MAPKs ERK1 and ERK2, which are physiological Bcl2 kinases. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 64-68 15447668-8 2004 In contrast to the effects of acute application of oligomeric beta-amyloid(1-42), nicotine activated ERK MAPK via alpha7 nicotinic acetylcholine receptors utilizing protein kinase A as an intermediate. Nicotine 82-90 mitogen-activated protein kinase 1 Homo sapiens 101-104 15447668-8 2004 In contrast to the effects of acute application of oligomeric beta-amyloid(1-42), nicotine activated ERK MAPK via alpha7 nicotinic acetylcholine receptors utilizing protein kinase A as an intermediate. Nicotine 82-90 mitogen-activated protein kinase 1 Homo sapiens 105-109 15447668-10 2004 We also found that nicotine and beta-amyloid activate ERK MAPK via alpha7 nicotinic acetylcholine receptors but use distinct intermediate kinases. Nicotine 19-27 mitogen-activated protein kinase 1 Homo sapiens 54-57 15447668-10 2004 We also found that nicotine and beta-amyloid activate ERK MAPK via alpha7 nicotinic acetylcholine receptors but use distinct intermediate kinases. Nicotine 19-27 mitogen-activated protein kinase 1 Homo sapiens 58-62 15733153-8 2005 A nicotine concentration of 5 mm was found to induce extracellular signal-regulated kinase (ERK) phosphorylation in a time-dependent manner (p<0.05). Nicotine 2-10 mitogen-activated protein kinase 1 Homo sapiens 92-95 15733153-11 2005 In addition, NS-398, dexamethasone, OTZ, herbimycin A, and curcumin were found to inhibit the nicotine-induced ERK expression (p<0.05). Nicotine 94-102 mitogen-activated protein kinase 1 Homo sapiens 111-114 15733153-12 2005 CONCLUSIONS: The activation of ERK expression by nicotine suggests a potential role for nicotine in the pathogenesis of cigarette smoking-associated periodontal disease. Nicotine 49-57 mitogen-activated protein kinase 1 Homo sapiens 31-34 15733153-12 2005 CONCLUSIONS: The activation of ERK expression by nicotine suggests a potential role for nicotine in the pathogenesis of cigarette smoking-associated periodontal disease. Nicotine 88-96 mitogen-activated protein kinase 1 Homo sapiens 31-34 15733153-13 2005 In addition, nicotine-induced ERK expression was down-regulated by NS-398, dexamethasone, OTZ, herbimycin A, and curcumin. Nicotine 13-21 mitogen-activated protein kinase 1 Homo sapiens 30-33 11905997-0 2002 Nicotine activates the extracellular signal-regulated kinase 1/2 via the alpha7 nicotinic acetylcholine receptor and protein kinase A, in SH-SY5Y cells and hippocampal neurones. Nicotine 0-8 mitogen-activated protein kinase 1 Homo sapiens 23-64 9600337-2 1998 The present study provides evidence that nicotine (a) activates the mitogen-activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal-regulated kinase (ERK2), resulting in increased expression of the bcl-2 protein and inhibition of apoptosis in these cells; and (b) blocks the inhibition of protein kinase C (PKC) and ERK2 activity in lung cancer cells by anti-cancer agents, such as therapeutic opioid drugs, and thus can adversely affect cancer therapy. Nicotine 41-49 mitogen-activated protein kinase 1 Homo sapiens 200-204 9600337-2 1998 The present study provides evidence that nicotine (a) activates the mitogen-activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal-regulated kinase (ERK2), resulting in increased expression of the bcl-2 protein and inhibition of apoptosis in these cells; and (b) blocks the inhibition of protein kinase C (PKC) and ERK2 activity in lung cancer cells by anti-cancer agents, such as therapeutic opioid drugs, and thus can adversely affect cancer therapy. Nicotine 41-49 mitogen-activated protein kinase 1 Homo sapiens 366-370 9600337-4 1998 While exposure to nicotine can result in the activation of the two major signalling pathways (MAP kinase and PKC) that are known to inhibit apoptosis, nicotine regulation of MAP (ERK2) kinase activity is not dependent on PKC. Nicotine 151-159 mitogen-activated protein kinase 1 Homo sapiens 179-183 34890707-10 2022 In this study, we found that nicotine induces IL-8 expression via ROS/NF-kappaB and ROS/MAPK (Erk1/2, p38)/AP-1 axis in gastric cancer cells, thus stimulating endothelial cell proliferation and angiogenesis in the tumor microenvironment. Nicotine 29-37 mitogen-activated protein kinase 1 Homo sapiens 102-105