PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25881894-9 2015 In the ethanol-treated cerebellar granule neurons we find an increased expression of genes related to apoptosis (Mapk8 and Bax), but also of genes previously described as neuroprotective (Dhcr24 and Bdnf), which might suggest an actively maintained viability. Ethanol 7-14 mitogen-activated protein kinase 8 Homo sapiens 113-118 23830200-0 2013 Expression of apoptosis-associated microRNAs in ethanol-induced acute gastric mucosal injury via JNK pathway. Ethanol 48-55 mitogen-activated protein kinase 8 Homo sapiens 97-100 25189124-8 2014 Moreover, signal transduction studies showed that COS was able to suppress the ethanol-induced phosphorylation of p38 MAPK, JNK and ERK. Ethanol 79-86 mitogen-activated protein kinase 8 Homo sapiens 124-127 23857333-8 2014 Ethanol suppressed arginine-methylation of FOXO3 promoting nuclear export and degradation of the JNK phosphorylated form. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 97-100 25393427-7 2014 Ethanol treatment specifically inhibited the activation of the ERK but not JNK nor the p38 MAP signaling pathway. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 75-78 25337571-5 2014 RESULTS: Ethanol induced time- and dose-dependent cell death in SK-N-SH cells and increased c-Jun N-terminal protein kinase (JNK) activity in a time- and concentration dependent manner. Ethanol 9-16 mitogen-activated protein kinase 8 Homo sapiens 92-123 25337571-5 2014 RESULTS: Ethanol induced time- and dose-dependent cell death in SK-N-SH cells and increased c-Jun N-terminal protein kinase (JNK) activity in a time- and concentration dependent manner. Ethanol 9-16 mitogen-activated protein kinase 8 Homo sapiens 125-128 25337571-7 2014 After treatment with JNK or p38 kinase inhibitors, ethanol-induced cell death significantly reduced. Ethanol 51-58 mitogen-activated protein kinase 8 Homo sapiens 21-24 25337571-10 2014 CONCLUSION: Our results suggest that ethanol mediates apoptosis of neuroblastoma cells by stimulating p53-related cell cycle arrest mediated through activation of the JNK-related pathway. Ethanol 37-44 mitogen-activated protein kinase 8 Homo sapiens 167-170 23830200-8 2013 In the human cell culture experiments, the anti-apoptotic effects of miR-19a and miR-21 or pro-apoptotic effect of miR-145 were confirmed by their corresponding mimics or inhibitor; the ethanol-induced GES-1 apoptosis as well as the changes in miRNAs expression were significantly attenuated in the presence of JNK inhibitor. Ethanol 186-193 mitogen-activated protein kinase 8 Homo sapiens 311-314 23830200-10 2013 The regulation of expression of these 3 miRNAs in ethanol-induced GES-1 apoptosis involved the JNK pathway. Ethanol 50-57 mitogen-activated protein kinase 8 Homo sapiens 95-98 23519123-0 2013 Regulation of cytochrome P450 2e1 expression by ethanol: role of oxidative stress-mediated pkc/jnk/sp1 pathway. Ethanol 48-55 mitogen-activated protein kinase 8 Homo sapiens 95-102 23726865-4 2013 Of three major MAPKs, only p38 MAPK and JNK were found activated by 200 mM ethanol treatment. Ethanol 75-82 mitogen-activated protein kinase 8 Homo sapiens 40-43 23726865-5 2013 When cells were incubated with inhibitors of p38 MAPK and JNK, ethanol-induced apoptosis was decreased while ROS generation was unaffected, and examination of pro-apoptotic Bax and anti-apoptotic Bcl-2 levels showed decrease of the former and increase of the latter. Ethanol 63-70 mitogen-activated protein kinase 8 Homo sapiens 58-61 23726865-6 2013 We concluded that oxidative stress inflicted by ROS triggered Fas-mediated and mitochondria-mediated apoptotic pathways in ethanol-treated SK-Hep1 cells, and that p38 MAPK and JNK were promoting mitochondrial pathway, suggesting interaction between apoptosis and MAPK signaling systems. Ethanol 123-130 mitogen-activated protein kinase 8 Homo sapiens 176-179 23454483-8 2013 Blocking the JNK1 pathway by a chemical inhibitor and siRNA reduces this ethanol-induced activity. Ethanol 73-80 mitogen-activated protein kinase 8 Homo sapiens 13-17 23519123-9 2013 In addition, inhibitors of JNK (SP600125) and SP1 (mithramycin A) completely abrogated induction of CYP2E1 by ethanol in SVGA astrocytes. Ethanol 110-117 mitogen-activated protein kinase 8 Homo sapiens 27-30 22454661-0 2012 Ethanol extracts of fruiting bodies of Antrodia cinnamomea suppress CL1-5 human lung adenocarcinoma cells migration by inhibiting matrix metalloproteinase-2/9 through ERK, JNK, p38, and PI3K/Akt signaling pathways. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 172-175 22722906-0 2013 Butein inhibits ethanol-induced activation of liver stellate cells through TGF-beta, NFkappaB, p38, and JNK signaling pathways and inhibition of oxidative stress. Ethanol 16-23 mitogen-activated protein kinase 8 Homo sapiens 104-107 22722906-7 2013 In ethanol-induced HSCs, butein inhibited the activation of the p38 MAPK and JNK transduction pathways as well as significantly inhibiting the phosphorylation of NF kappaB inhibitor (IkappaB) and Smad3. Ethanol 3-10 mitogen-activated protein kinase 8 Homo sapiens 77-80 23054611-9 2013 In addition, ethanol markedly stimulates phosphorylation of JNK1, but not JNK2. Ethanol 13-20 mitogen-activated protein kinase 8 Homo sapiens 60-64 17590997-5 2007 Ethanol and acetaldehyde activatedJNK have opposing roles; ethanol-induced JNK activation increased apoptosis whereas that by acetaldehyde decreased apoptosis. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 34-37 21034468-12 2010 C3G abolished ethanol-mediated p130(Cas)/JNK interaction. Ethanol 14-21 mitogen-activated protein kinase 8 Homo sapiens 41-44 17848570-0 2007 Role of MAPK phosphatase-1 in sustained activation of JNK during ethanol-induced apoptosis in hepatocyte-like VL-17A cells. Ethanol 65-72 mitogen-activated protein kinase 8 Homo sapiens 54-57 17848570-4 2007 The aim of the study is to evaluate the role of MKP-1 in sustained JNK activation as a mechanism to explain ethanol-induced hepatocyte apoptosis. Ethanol 108-115 mitogen-activated protein kinase 8 Homo sapiens 67-70 17848570-10 2007 Ethanol incubation markedly decreased the MKP-1 protein levels to 15% of control levels and was associated with sustained phosphorylation of p46 JNK and p54 JNK, as well as increased apoptosis. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 145-148 17848570-10 2007 Ethanol incubation markedly decreased the MKP-1 protein levels to 15% of control levels and was associated with sustained phosphorylation of p46 JNK and p54 JNK, as well as increased apoptosis. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 157-160 17640761-0 2007 Stabilization of IGFBP-1 mRNA by ethanol in hepatoma cells involves the JNK pathway. Ethanol 33-40 mitogen-activated protein kinase 8 Homo sapiens 72-75 17640761-8 2007 Ethanol triggered a rapid activation of c-Jun N-terminal Kinase (JNK) in HepG2 cells and IGFBP-1 induction was significantly decreased by a specific inhibitor of JNK. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 40-63 17640761-8 2007 Ethanol triggered a rapid activation of c-Jun N-terminal Kinase (JNK) in HepG2 cells and IGFBP-1 induction was significantly decreased by a specific inhibitor of JNK. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 65-68 17640761-8 2007 Ethanol triggered a rapid activation of c-Jun N-terminal Kinase (JNK) in HepG2 cells and IGFBP-1 induction was significantly decreased by a specific inhibitor of JNK. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 162-165 18521936-7 2008 Pretreatment with JNK inhibitor (SP600125) of SH-SY5Y cells inhibited JNK phosphorylation and interaction between p-JNK and 14-3-3 resulting from ethanol. Ethanol 146-153 mitogen-activated protein kinase 8 Homo sapiens 18-21 18521936-7 2008 Pretreatment with JNK inhibitor (SP600125) of SH-SY5Y cells inhibited JNK phosphorylation and interaction between p-JNK and 14-3-3 resulting from ethanol. Ethanol 146-153 mitogen-activated protein kinase 8 Homo sapiens 70-73 18595723-3 2008 To explore lithium"s mechanism of action, we focused on kinase signaling systems (ERK, Akt, JNK) that are believed to play a regulatory role in cell survival, and found that very rapidly after ethanol administration there is a suppression of ERK phosphorylation, and that lithium stimulates ERK phosphorylation and prevents ethanol from suppressing this phosphorylation process. Ethanol 193-200 mitogen-activated protein kinase 8 Homo sapiens 92-95 18595723-5 2008 We also found that ethanol activates the JNK system, but this cannot explain the neurotoxic action of ethanol, because JNK activation did not occur in the same neuronal populations that are killed by ethanol. Ethanol 19-26 mitogen-activated protein kinase 8 Homo sapiens 41-44 17848570-12 2007 Ethanol-induced oxidative stress enhanced the tyrosine phosphorylation of PKCdelta, which in turn caused the proteasomal degradation of MKP-1, leading to sustained JNK activation and increased apoptosis in VL-17A cells. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 164-167 17590997-5 2007 Ethanol and acetaldehyde activatedJNK have opposing roles; ethanol-induced JNK activation increased apoptosis whereas that by acetaldehyde decreased apoptosis. Ethanol 59-66 mitogen-activated protein kinase 8 Homo sapiens 34-37 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 54-58 mitogen-activated protein kinase 8 Homo sapiens 2-23 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 54-58 mitogen-activated protein kinase 8 Homo sapiens 25-28 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 54-58 mitogen-activated protein kinase 8 Homo sapiens 171-174 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 122-129 mitogen-activated protein kinase 8 Homo sapiens 2-23 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 122-129 mitogen-activated protein kinase 8 Homo sapiens 25-28 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 122-129 mitogen-activated protein kinase 8 Homo sapiens 171-174 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 178-182 mitogen-activated protein kinase 8 Homo sapiens 2-23 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 178-182 mitogen-activated protein kinase 8 Homo sapiens 25-28 17113937-5 2006 A jun N-terminal kinase (JNK) pathway is activated by EtOH and their pharmacological inhibition (by SP600125) neutralized ethanol-induced apoptosis, suggesting a role for JNK in EtOH neurotoxicity. Ethanol 178-182 mitogen-activated protein kinase 8 Homo sapiens 171-174 17113937-7 2006 Examination of the cytoskeleton showed that EtOH depolymerized actin filaments, inducing p-JNK dissociation and translocation to the nucleus, which suggests that released p-JNK may contribute to glial cell death after EtOH exposure. Ethanol 44-48 mitogen-activated protein kinase 8 Homo sapiens 91-94 17113937-7 2006 Examination of the cytoskeleton showed that EtOH depolymerized actin filaments, inducing p-JNK dissociation and translocation to the nucleus, which suggests that released p-JNK may contribute to glial cell death after EtOH exposure. Ethanol 44-48 mitogen-activated protein kinase 8 Homo sapiens 173-176 17113937-7 2006 Examination of the cytoskeleton showed that EtOH depolymerized actin filaments, inducing p-JNK dissociation and translocation to the nucleus, which suggests that released p-JNK may contribute to glial cell death after EtOH exposure. Ethanol 218-222 mitogen-activated protein kinase 8 Homo sapiens 173-176 16609996-9 2006 CONCLUSION: The JNK signaling cascade is a key component of the proapoptotic signaling pathway induced by ethanol. Ethanol 106-113 mitogen-activated protein kinase 8 Homo sapiens 16-19 16609996-0 2006 S-adenosyl-methionine decreases ethanol-induced apoptosis in primary hepatocyte cultures by a c-Jun N-terminal kinase activity-independent mechanism. Ethanol 32-39 mitogen-activated protein kinase 8 Homo sapiens 94-117 16609996-1 2006 AIM: To determine the role of c-Jun N-terminal kinase (JNK) activity in ethanol-induced apoptosis and the modulation of this signaling cascade by S-Adenosyl-methionine (AdoMet). Ethanol 72-79 mitogen-activated protein kinase 8 Homo sapiens 30-53 16609996-1 2006 AIM: To determine the role of c-Jun N-terminal kinase (JNK) activity in ethanol-induced apoptosis and the modulation of this signaling cascade by S-Adenosyl-methionine (AdoMet). Ethanol 72-79 mitogen-activated protein kinase 8 Homo sapiens 55-58 16609996-7 2006 RESULTS: The exposure of hepatocytes to ethanol induced JNK activation, c-jun phosphorylation, Bid fragmentation, cytochrome c release and pro-caspase 3 cleavage; these effects were diminished by SP600125, and caused a significant decrease in ethanol-induced apoptosis (P< 0.05). Ethanol 40-47 mitogen-activated protein kinase 8 Homo sapiens 56-59 10675770-9 2000 Additionally, ethanol specifically induced phosphorylation of c-jun N-terminal-kinase (JNK), a mitogen-activated protein (MAP) kinase selectively associated with apoptosis. Ethanol 14-21 mitogen-activated protein kinase 8 Homo sapiens 62-85 15976518-10 2005 Furthermore, exposure to ethanol potentiated and prolonged agonist-induced activation of JNK. Ethanol 25-32 mitogen-activated protein kinase 8 Homo sapiens 89-92 15976518-11 2005 Inhibition of JNK by over-expression of dominant negative JNK1 substantially reversed ethanol/TNF-mediated inhibition of cyclin A expression and EC proliferation, suggesting modulation of JNK1 signaling as the mechanism for ethanol/TNF-induced EC dysfunctions. Ethanol 86-93 mitogen-activated protein kinase 8 Homo sapiens 14-17 15976518-11 2005 Inhibition of JNK by over-expression of dominant negative JNK1 substantially reversed ethanol/TNF-mediated inhibition of cyclin A expression and EC proliferation, suggesting modulation of JNK1 signaling as the mechanism for ethanol/TNF-induced EC dysfunctions. Ethanol 86-93 mitogen-activated protein kinase 8 Homo sapiens 58-62 15976518-11 2005 Inhibition of JNK by over-expression of dominant negative JNK1 substantially reversed ethanol/TNF-mediated inhibition of cyclin A expression and EC proliferation, suggesting modulation of JNK1 signaling as the mechanism for ethanol/TNF-induced EC dysfunctions. Ethanol 86-93 mitogen-activated protein kinase 8 Homo sapiens 188-192 15189113-5 2004 In response to ethanol exposure, specific signal transduction pathways, including NFkappaB and the mitogen-activated protein kinase family members ERK1/2, JNK, and p38, are activated. Ethanol 15-22 mitogen-activated protein kinase 8 Homo sapiens 155-158 10832914-5 2000 RESULTS: Ethanol-treated PNET2 neuronal cells exhibited increased apoptosis mediated by increased levels of p53 and phospho-amino-terminal c-jun kinase (phospho-JNK), and reduced levels of Bcl-2, phosphoinositol 3-kinase (PI3 K), and intact (approximately 116 kD) poly (ADP ribose) polymerase (PARP), a deoxyribonucleic acid repair enzyme and important substrate for caspase 3. Ethanol 9-16 mitogen-activated protein kinase 8 Homo sapiens 161-164 16272348-6 2005 We show in this study that ethanol, at physiologically relevant concentrations, is capable of inducing rapid phosphorylation within 10 min of IL-1R-associated kinase, ERK1/2, stress-activated protein kinase/JNK, and p38 MAPK in astrocytes. Ethanol 27-34 mitogen-activated protein kinase 8 Homo sapiens 207-210 15027449-11 2004 Acute exposure to ethanol activates pro-apoptotic JNK pathway and anti-apoptotic p42/44 MAPK pathway. Ethanol 18-25 mitogen-activated protein kinase 8 Homo sapiens 50-53 14713309-4 2003 Cell death induced by ethanol is associated with stimulation of neutral and acidic sphingomyelinase (SMase) and ceramide generation, as well as with activation of stress-related kinases, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38) and extracellular signal-regulated kinase (ERK) pathways. Ethanol 22-29 mitogen-activated protein kinase 8 Homo sapiens 187-210 14713309-4 2003 Cell death induced by ethanol is associated with stimulation of neutral and acidic sphingomyelinase (SMase) and ceramide generation, as well as with activation of stress-related kinases, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38) and extracellular signal-regulated kinase (ERK) pathways. Ethanol 22-29 mitogen-activated protein kinase 8 Homo sapiens 212-215 14713309-5 2003 We also provide evidence for the participation of JNK and p38 in ethanol-induced cell death, because pharmacological inhibitors of these kinases largely prevent the apoptosis induced by ethanol or by ethanol and C2-ceramide. Ethanol 65-72 mitogen-activated protein kinase 8 Homo sapiens 50-53 14713309-5 2003 We also provide evidence for the participation of JNK and p38 in ethanol-induced cell death, because pharmacological inhibitors of these kinases largely prevent the apoptosis induced by ethanol or by ethanol and C2-ceramide. Ethanol 186-193 mitogen-activated protein kinase 8 Homo sapiens 50-53 14713309-5 2003 We also provide evidence for the participation of JNK and p38 in ethanol-induced cell death, because pharmacological inhibitors of these kinases largely prevent the apoptosis induced by ethanol or by ethanol and C2-ceramide. Ethanol 186-193 mitogen-activated protein kinase 8 Homo sapiens 50-53 10675770-9 2000 Additionally, ethanol specifically induced phosphorylation of c-jun N-terminal-kinase (JNK), a mitogen-activated protein (MAP) kinase selectively associated with apoptosis. Ethanol 14-21 mitogen-activated protein kinase 8 Homo sapiens 87-90 10082520-5 1999 Conversely, exposure of cells to heat shock and other protein-damaging conditions, including ethanol, arsenite, and oxidative stress, strongly reduced the rate of JNK dephosphorylation. Ethanol 93-100 mitogen-activated protein kinase 8 Homo sapiens 163-166 35455080-0 2022 Euphorbia hirta Leaf Ethanol Extract Suppresses TNF-alpha/IFN-gamma-Induced Inflammatory Response via Down-Regulating JNK or STAT1/3 Pathways in Human Keratinocytes. Ethanol 21-28 mitogen-activated protein kinase 8 Homo sapiens 118-121 9497367-10 1998 Accordingly, pretreatment with MG132 reduced JNK-dependent apoptosis caused by heat shock or ethanol, but it was unable to block JNK-independent apoptosis induced by TNFalpha. Ethanol 93-100 mitogen-activated protein kinase 8 Homo sapiens 45-48 34821900-6 2021 Meanwhile, sterol pretreatment groups down-regulated the protein expression levels of p-P38 and p-JNK in ethanol-damaged GES-1 cells and up-regulated the expression level of p-ERK, suggesting that sterols protect GES-1 cells from ethanol-induced damage by regulating the MAPK signaling pathway. Ethanol 105-112 mitogen-activated protein kinase 8 Homo sapiens 98-101 33690904-7 2021 An oxidative stress and ER stress as measured by GRP78, unspliced XBP1, p-eIF2alpha, and CHOP along with activation of p-JNK1/2, p-ERK1/2, and p-P38MAPK were found in cells treated with EtOH, acetaldehyde or FAEEs were increased concentration dependently. Ethanol 186-190 mitogen-activated protein kinase 8 Homo sapiens 121-127 33791043-14 2021 These effects are associated with the reduced activation of JNK/STAT3 by EtOH, particularly in the condition of acute exposure to low-dose EtOH. Ethanol 73-77 mitogen-activated protein kinase 8 Homo sapiens 60-63 33791043-14 2021 These effects are associated with the reduced activation of JNK/STAT3 by EtOH, particularly in the condition of acute exposure to low-dose EtOH. Ethanol 139-143 mitogen-activated protein kinase 8 Homo sapiens 60-63 32787872-11 2020 Ethanol-increased NMDAR induced intracellular calcium overload and calmodulin-dependent protein kinase II (CaMKII) activation leading to phosphorylation of dynamin-related protein 1 (Drp1) and c-Jun N-terminal protein kinase 1 (JNK1). Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 193-226 32787872-11 2020 Ethanol-increased NMDAR induced intracellular calcium overload and calmodulin-dependent protein kinase II (CaMKII) activation leading to phosphorylation of dynamin-related protein 1 (Drp1) and c-Jun N-terminal protein kinase 1 (JNK1). Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 228-232 32787872-13 2020 Ethanol-induced JNK1 phosphorylation activated the NLRP3 inflammasome that induced caspase-1 dependent mitophagy inhibition, thereby exacerbating ROS accumulation and causing cell death. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 16-20 32787872-15 2020 CONCLUSIONS: Our results demonstrated that ethanol upregulated NMDAR-dependent CaMKII phosphorylation which is essential for Drp1-mediated excessive mitochondrial fission and the JNK1-induced NLRP3 inflammasome activation resulting in neuronal apoptosis. Ethanol 43-50 mitogen-activated protein kinase 8 Homo sapiens 179-183 30106096-9 2018 The results of the present study demonstrated that treatment with ethanol inhibited GES-1 cell proliferation, and enhanced ROS levels and apoptosis rates, potentially via downregulation of B-cell lymphoma-2 (Bcl-2) expression and upregulation of Bcl-2-associated X and caspase-3 expression levels, as well as enhancing the phosphorylation levels of ERK, JNK and p38. Ethanol 66-73 mitogen-activated protein kinase 8 Homo sapiens 354-357 29336467-9 2018 Ethanol-induced apoptosis and cell death of L-02 cells was accompanied by the generation of ROS, elevated expression of NOX, as well as phosphorylation of JNK and P-38. Ethanol 0-7 mitogen-activated protein kinase 8 Homo sapiens 155-158 28965650-11 2017 Furthermore, JNK phosphorylation in ethanol-treated human umbilical vein endothelial cells was suppressed even in the presence of exogenous TNF-alpha, resulting in inhibition of PTX3 mRNA and protein expression. Ethanol 36-43 mitogen-activated protein kinase 8 Homo sapiens 13-16 28062356-2 2017 Cytotoxicity, ROS production, and JNK and ERK1/2 kinase signaling increased in a dose and time-dependent manner during ethanol treatments; CYP4F2 gene expression decreased, while other CYP4F forms, namely 4F11 and 12, increased along with 3A4 and 2E1 isoforms. Ethanol 119-126 mitogen-activated protein kinase 8 Homo sapiens 34-37 33106514-5 2020 Additionally, [Cu(PMPP-SAL)(EtOH)] inhibited the PI3K/AKT pathway and activated the P38/MAPK, and JNK/MAPK pathways. Ethanol 28-32 mitogen-activated protein kinase 8 Homo sapiens 98-106 29807029-4 2018 mTOR, JNK and PI3K intracellular signaling pathways were involved in the effect of EtOH upon 3H-FA uptake and in the effect of METF upon cell viability, and mTOR and JNK in the effect of EtOH upon cell viability and 3H-DG uptake. Ethanol 83-87 mitogen-activated protein kinase 8 Homo sapiens 6-9 29807029-4 2018 mTOR, JNK and PI3K intracellular signaling pathways were involved in the effect of EtOH upon 3H-FA uptake and in the effect of METF upon cell viability, and mTOR and JNK in the effect of EtOH upon cell viability and 3H-DG uptake. Ethanol 187-191 mitogen-activated protein kinase 8 Homo sapiens 166-169 28608757-9 2018 In neutrophils exposed to ethanol or NDMA was observed an increased NF-kappaB-dependent NO production mediated by iNOS with the contribution of MAP kinases: p38 and JNK. Ethanol 26-33 mitogen-activated protein kinase 8 Homo sapiens 165-168 28400856-11 2017 CONCLUSION: Glossogyne tenuifolia ethanol extract inhibited T cell activation of Jurkat cells and freshly prepared human PBMCs due to suppression of JNK activity. Ethanol 34-41 mitogen-activated protein kinase 8 Homo sapiens 149-152 26470730-4 2016 In this study we demonstrate that exposure of hepatocytes to ethanol or exposure of macrophages to lipopolysaccharide (LPS) induces the c-Jun N-terminal kinase (JNK)-dependent phosphorylation of FOXO3 at serine-574. Ethanol 61-68 mitogen-activated protein kinase 8 Homo sapiens 136-159 26470730-4 2016 In this study we demonstrate that exposure of hepatocytes to ethanol or exposure of macrophages to lipopolysaccharide (LPS) induces the c-Jun N-terminal kinase (JNK)-dependent phosphorylation of FOXO3 at serine-574. Ethanol 61-68 mitogen-activated protein kinase 8 Homo sapiens 161-164