PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35624743-8 2022 Furthermore, we found that DDAH1 knockdown aggravated APAP-induced cell death, oxidative stress, phosphorylation of JNK and p65, upregulation of CYP2E1 and downregulation of GSTA1 in HepG2 cells. Acetaminophen 54-58 mitogen-activated protein kinase 8 Homo sapiens 116-119 11562448-9 2001 Transfection of cDNA for the dominant-negative mutant JNK-KR or stress-activated protein kinase kinase-1 Lys-->Arg mutant (SEK1-KR), an immediate upstream kinase of JNK, significantly reduced AAP-induced JNK activation and cell death rate. Acetaminophen 195-198 mitogen-activated protein kinase 8 Homo sapiens 54-57 11562448-9 2001 Transfection of cDNA for the dominant-negative mutant JNK-KR or stress-activated protein kinase kinase-1 Lys-->Arg mutant (SEK1-KR), an immediate upstream kinase of JNK, significantly reduced AAP-induced JNK activation and cell death rate. Acetaminophen 195-198 mitogen-activated protein kinase 8 Homo sapiens 168-171 11562448-9 2001 Transfection of cDNA for the dominant-negative mutant JNK-KR or stress-activated protein kinase kinase-1 Lys-->Arg mutant (SEK1-KR), an immediate upstream kinase of JNK, significantly reduced AAP-induced JNK activation and cell death rate. Acetaminophen 195-198 mitogen-activated protein kinase 8 Homo sapiens 168-171 11562448-11 2001 Pretreatment with YH439, an inhibitor of CYP2E1 gene transcription, markedly reduced CYP2E1 mRNA, protein content, and activity, as well as the rate of AAP-induced JNK activation and cell death. Acetaminophen 152-155 mitogen-activated protein kinase 8 Homo sapiens 164-167 32617995-0 2021 Does JNK Regulate Acetaminophen Hepatotoxicity by Modulating Nrf2-dependent Genes or Mitochondrial Oxidant Stress? Acetaminophen 18-31 mitogen-activated protein kinase 8 Homo sapiens 5-8 33959992-5 2021 The results showed that inhibiting JNK could ameliorate APAP-induced hepatocyte injury, reduced oxidative stress, suppressed JNK and c-Jun activation, and hepatocyte apoptosis. Acetaminophen 56-60 mitogen-activated protein kinase 8 Homo sapiens 35-38 33959992-5 2021 The results showed that inhibiting JNK could ameliorate APAP-induced hepatocyte injury, reduced oxidative stress, suppressed JNK and c-Jun activation, and hepatocyte apoptosis. Acetaminophen 56-60 mitogen-activated protein kinase 8 Homo sapiens 125-128 35145060-7 2022 Transcriptional and translational activation of the UPR and sustained activation of JNK1/2 were major events in APAP hepatotoxicity, both in a human hepatocytic cell line and in a preclinical model. Acetaminophen 112-116 mitogen-activated protein kinase 8 Homo sapiens 84-90 35145060-8 2022 Xbp1 hepa livers showed decreased UPR and JNK1/2 activation but enhanced autophagy in response to high dose APAP. Acetaminophen 108-112 mitogen-activated protein kinase 8 Homo sapiens 42-48 33983442-4 2021 While a sequence of molecular events involving formation of the reactive metabolite N-acetyl-p-benzoquinone imine, GSH depletion, oxidative stress, and JNK activation define the early cell stress trajectory following APAP exposure, their activation in PC vs PP hepatocytes is not well characterized. Acetaminophen 217-221 mitogen-activated protein kinase 8 Homo sapiens 152-155 31212128-0 2019 Mangiferin ameliorates acetaminophen-induced hepatotoxicity through APAP-Cys and JNK modulation. Acetaminophen 23-36 mitogen-activated protein kinase 8 Homo sapiens 81-84 30974967-14 2019 Our findings suggest that TQ may actively prevent APAP-induced acute liver injury, and the effect may be mediated by JNK and AMPK signaling pathways. Acetaminophen 50-54 mitogen-activated protein kinase 8 Homo sapiens 117-120 30630510-11 2019 In vivo, Cori significantly protected against APAP-induced ALF by reducing mortality and alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, attenuating histopathological liver changes, inhibiting myeloperoxidase (MPO) and malondialdehyde (MDA) levels, and increasing the superoxide dismutase (SOD) content and GSH-to-GSSG ratio as well as suppressing c-jun N-terminal kinase (JNK) phosphorylation. Acetaminophen 46-50 mitogen-activated protein kinase 8 Homo sapiens 372-395 30630510-11 2019 In vivo, Cori significantly protected against APAP-induced ALF by reducing mortality and alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, attenuating histopathological liver changes, inhibiting myeloperoxidase (MPO) and malondialdehyde (MDA) levels, and increasing the superoxide dismutase (SOD) content and GSH-to-GSSG ratio as well as suppressing c-jun N-terminal kinase (JNK) phosphorylation. Acetaminophen 46-50 mitogen-activated protein kinase 8 Homo sapiens 397-400 26998291-11 2016 Furthermore, we identified 4 molecular signaling pathways associated with acetaminophen response that may also affect overall survival in women with OVCA, including the JNK pathway, which has been previously implicated in the mechanism of action of acetaminophen and is predictive of decreased survival in women with OVCA. Acetaminophen 74-87 mitogen-activated protein kinase 8 Homo sapiens 169-172 29739258-6 2018 In addition, 4MP largely prevented APAP-induced activation of c-Jun N-terminal kinase (JNK), mitochondrial translocation of phospho-JNK and Bax, and the release of mitochondrial intermembrane proteins. Acetaminophen 35-39 mitogen-activated protein kinase 8 Homo sapiens 62-85 29739258-6 2018 In addition, 4MP largely prevented APAP-induced activation of c-Jun N-terminal kinase (JNK), mitochondrial translocation of phospho-JNK and Bax, and the release of mitochondrial intermembrane proteins. Acetaminophen 35-39 mitogen-activated protein kinase 8 Homo sapiens 87-90 29739258-6 2018 In addition, 4MP largely prevented APAP-induced activation of c-Jun N-terminal kinase (JNK), mitochondrial translocation of phospho-JNK and Bax, and the release of mitochondrial intermembrane proteins. Acetaminophen 35-39 mitogen-activated protein kinase 8 Homo sapiens 132-135 27562556-14 2016 Furthermore, the protection was reproduced in JNK activation-absent HepaRG cells treated with 20 mM APAP followed by 0.5 or 1 mM metformin 6 h later, confirming JNK-independent protection mechanisms. Acetaminophen 100-104 mitogen-activated protein kinase 8 Homo sapiens 46-49 27562556-14 2016 Furthermore, the protection was reproduced in JNK activation-absent HepaRG cells treated with 20 mM APAP followed by 0.5 or 1 mM metformin 6 h later, confirming JNK-independent protection mechanisms. Acetaminophen 100-104 mitogen-activated protein kinase 8 Homo sapiens 161-164 27375192-0 2016 Mechanisms of Acetaminophen Hepatotoxicity: Do We Need JNK for Cell Death? Acetaminophen 14-27 mitogen-activated protein kinase 8 Homo sapiens 55-58 27165078-1 2016 Acetaminophen in a concentration of 5 mM increased the expression of JNK, HIF1A (hypoxiainduced factor), and CASP3, which indicated development of oxidative stress and apoptotic cell death. Acetaminophen 0-13 mitogen-activated protein kinase 8 Homo sapiens 69-72 26998291-11 2016 Furthermore, we identified 4 molecular signaling pathways associated with acetaminophen response that may also affect overall survival in women with OVCA, including the JNK pathway, which has been previously implicated in the mechanism of action of acetaminophen and is predictive of decreased survival in women with OVCA. Acetaminophen 249-262 mitogen-activated protein kinase 8 Homo sapiens 169-172 26190663-0 2015 Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity. Acetaminophen 62-75 mitogen-activated protein kinase 8 Homo sapiens 35-58 25204659-4 2014 In APAP-treated human hepatocytes at concentrations that did not induce death, phosphorylation of JNK and PTP1B expression and enzymatic activity were increased. Acetaminophen 3-7 mitogen-activated protein kinase 8 Homo sapiens 98-101 17185352-5 2007 RESULTS: Paracetamol-induced hepatic JNK activation both in human and murine paracetamol hepatotoxicity and in our murine model preceded the onset of hepatocyte death. Acetaminophen 9-20 mitogen-activated protein kinase 8 Homo sapiens 37-40 24905542-9 2014 Both co-treatment and post-treatment (3h) with the JNK inhibitor SP600125 reduced JNK activation and significantly attenuated cell death at 24h and 48h after APAP. Acetaminophen 158-162 mitogen-activated protein kinase 8 Homo sapiens 51-54 24492462-4 2014 We demonstrated that treatment of APAP in NCP-cultured HepG2 cells shows key mechanistic features of APAP-induced hepatotoxicity, such as decreases in intracellular glutathione and mitochondrial membrane potential, activation of JNK, and cellular injury; and pharmacological agents, such as Cyclosporine A (a mitochondrial permeability transition inhibitor) and SP600125 (a JNK inhibitor), prevented cell injury induced by APAP exposure. Acetaminophen 34-38 mitogen-activated protein kinase 8 Homo sapiens 229-232 24492462-4 2014 We demonstrated that treatment of APAP in NCP-cultured HepG2 cells shows key mechanistic features of APAP-induced hepatotoxicity, such as decreases in intracellular glutathione and mitochondrial membrane potential, activation of JNK, and cellular injury; and pharmacological agents, such as Cyclosporine A (a mitochondrial permeability transition inhibitor) and SP600125 (a JNK inhibitor), prevented cell injury induced by APAP exposure. Acetaminophen 34-38 mitogen-activated protein kinase 8 Homo sapiens 374-377 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 0-13 mitogen-activated protein kinase 8 Homo sapiens 90-113 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 0-13 mitogen-activated protein kinase 8 Homo sapiens 115-118 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 15-19 mitogen-activated protein kinase 8 Homo sapiens 90-113 20423716-1 2010 Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Acetaminophen 15-19 mitogen-activated protein kinase 8 Homo sapiens 115-118 20423716-11 2010 Our data suggest that the JNK inhibitor SP600125 protects against APAP-induced liver injury in part by attenuation of mitochondrial Bax translocation but mainly by preventing mitochondrial oxidant stress and peroxynitrite formation and thereby preventing the mitochondrial permeability transition pore opening, a key event in APAP-induced cell necrosis. Acetaminophen 66-70 mitogen-activated protein kinase 8 Homo sapiens 26-29 20166895-0 2010 Acetaminophen induced acute liver failure via oxidative stress and JNK activation: protective role of taurine by the suppression of cytochrome P450 2E1. Acetaminophen 0-13 mitogen-activated protein kinase 8 Homo sapiens 67-70 20166895-5 2010 APAP overdose caused injury in the hepatic tissue and hepatocytes via the upregulation of CYP2E1 and JNK. Acetaminophen 0-4 mitogen-activated protein kinase 8 Homo sapiens 101-104 20166895-7 2010 Results indicate that APAP overdose caused hepatic injury due to its metabolism to hepatotoxic NAPQI (N-acetyl-p-benzoquinone imine), usually catalysed by CYP2E1, and via the direct activation of JNK-dependent cell death pathway. Acetaminophen 22-26 mitogen-activated protein kinase 8 Homo sapiens 196-199 19931551-5 2010 ER redox alterations and early ER-stress-related signaling events induced by acetaminophen, such as ER glutathione depletion, phosphorylation of eIF2alpha and JNK and induction of the transcription factor GADD153, were not counteracted by co-treatment with BGP-15. Acetaminophen 77-90 mitogen-activated protein kinase 8 Homo sapiens 159-162 17185352-5 2007 RESULTS: Paracetamol-induced hepatic JNK activation both in human and murine paracetamol hepatotoxicity and in our murine model preceded the onset of hepatocyte death. Acetaminophen 77-88 mitogen-activated protein kinase 8 Homo sapiens 37-40 16979204-0 2006 Leflunomide or A77 1726 protect from acetaminophen-induced cell injury through inhibition of JNK-mediated mitochondrial permeability transition in immortalized human hepatocytes. Acetaminophen 37-50 mitogen-activated protein kinase 8 Homo sapiens 93-96 16979204-8 2006 Instead, we demonstrate that leflunomide (20 microM) inhibited the APAP-induced early (3 h) activation (phosphorylation) of JNK1/2, thus inhibiting phosphorylation of the anti-apoptotic protein Bcl-2 and preventing P-Bcl-2-mediated induction of the mPT. Acetaminophen 67-71 mitogen-activated protein kinase 8 Homo sapiens 124-130