PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27838438-10 2016 Reducing JNK expression (siJNK) increased extracellular O2 - suggesting that JNK provides important negative feedback regulation to Nox1 at the plasma membrane. Superoxides 56-58 mitogen-activated protein kinase 8 Homo sapiens 9-12 32014500-6 2020 The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO and O2 -) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). Superoxides 25-27 mitogen-activated protein kinase 8 Homo sapiens 284-309 32014500-6 2020 The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO and O2 -) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). Superoxides 25-27 mitogen-activated protein kinase 8 Homo sapiens 311-314 27181592-9 2017 Additionally, inhibition of JNK with SP600125 alleviated intracellular accumulation of ROS and attenuated mitochondrial generation of superoxide. Superoxides 134-144 mitogen-activated protein kinase 8 Homo sapiens 28-31 34826531-6 2022 Meanwhile, Au NS exhibited enhanced ROS scavenging efficiency of hydrogen peroxides and superoxide, which was helpful to restrain the activity of peroxisome proliferators-activated receptors beta (PPARbeta) and c-Jun N-terminal kinase (JNK), thereby reducing HSCs proliferation to enhance HSCs inactivation efficacy. Superoxides 88-98 mitogen-activated protein kinase 8 Homo sapiens 211-234 34826531-6 2022 Meanwhile, Au NS exhibited enhanced ROS scavenging efficiency of hydrogen peroxides and superoxide, which was helpful to restrain the activity of peroxisome proliferators-activated receptors beta (PPARbeta) and c-Jun N-terminal kinase (JNK), thereby reducing HSCs proliferation to enhance HSCs inactivation efficacy. Superoxides 88-98 mitogen-activated protein kinase 8 Homo sapiens 236-239 33732696-6 2021 The pharmacological dissociation of the GSTP1-JNK heterocomplex resulted in the activation of JNK, which led to a significant decrease in sperm viability, motility, mitochondrial activity, and plasma membrane stability, as well as to an increase of intracellular superoxides. Superoxides 263-274 mitogen-activated protein kinase 8 Homo sapiens 46-49 33732696-6 2021 The pharmacological dissociation of the GSTP1-JNK heterocomplex resulted in the activation of JNK, which led to a significant decrease in sperm viability, motility, mitochondrial activity, and plasma membrane stability, as well as to an increase of intracellular superoxides. Superoxides 263-274 mitogen-activated protein kinase 8 Homo sapiens 94-97 31759978-6 2020 Increased production of O2 - after X1 or sorafenib was abrogated by JNK inhibition and antioxidants. Superoxides 24-26 mitogen-activated protein kinase 8 Homo sapiens 68-71 29207156-0 2018 MAPK inhibitors, particularly the JNK inhibitor, increase cell death effects in H2O2-treated lung cancer cells via increased superoxide anion and glutathione depletion. Superoxides 125-141 mitogen-activated protein kinase 8 Homo sapiens 34-37 29207156-6 2018 Intracellular ROS levels were significantly increased in the H2O2-treated cells at 1 and 24 h. Only the JNK inhibitor increased ROS levels in the H2O2-treated cells at 1 h and all MAPK inhibitors raised superoxide anion levels in these cells at 24 h. In addition, H2O2 induced GSH depletion in Calu-6 and A549 cells and the JNK inhibitor significantly enhanced GSH depletion in H2O2-treated cells. Superoxides 203-219 mitogen-activated protein kinase 8 Homo sapiens 104-107 29207156-9 2018 The enhanced effect of MAPK inhibitors, especially the JNK inhibitor, on cell death in H2O2-treated lung cancer cells was correlated with increased O2 - levels and GSH depletion. Superoxides 89-91 mitogen-activated protein kinase 8 Homo sapiens 55-58 29183043-8 2017 Conclusions: B(e)P decreases the endothelium-dependent NO-induced vasodilation in the retinal arterioles through the production of superoxide from NADPH oxidase, which is linked to JNK and p38 kinase. Superoxides 131-141 mitogen-activated protein kinase 8 Homo sapiens 181-184 27838438-10 2016 Reducing JNK expression (siJNK) increased extracellular O2 - suggesting that JNK provides important negative feedback regulation to Nox1 at the plasma membrane. Superoxides 56-58 mitogen-activated protein kinase 8 Homo sapiens 27-30 26001727-10 2015 TNFalpha-stimulated superoxide generation was enhanced by JNK1 inhibition in WT, but not in Nox1 KO VSMC. Superoxides 20-30 mitogen-activated protein kinase 8 Homo sapiens 58-62 25285524-6 2014 Oxidative stress from menadione-generated superoxide induced JNK-dependent stathmin phosphorylation at Ser-16, Ser-25 and Ser-38 in hepatocytes. Superoxides 42-52 mitogen-activated protein kinase 8 Homo sapiens 61-64 22222766-4 2012 The c-Jun N-terminal kinase (JNK) was potently activated after superoxide accumulation. Superoxides 63-73 mitogen-activated protein kinase 8 Homo sapiens 4-27 24407242-4 2014 P-JNK plus adenosine 5"-triphosphate (ATP) added to isolated liver mitochondria promoted superoxide production, which was amplified by addition of calcium and inhibited by a blocking peptide corresponding to the JNK binding site on Sab (KIM1). Superoxides 89-99 mitogen-activated protein kinase 8 Homo sapiens 2-5 24407242-4 2014 P-JNK plus adenosine 5"-triphosphate (ATP) added to isolated liver mitochondria promoted superoxide production, which was amplified by addition of calcium and inhibited by a blocking peptide corresponding to the JNK binding site on Sab (KIM1). Superoxides 89-99 mitogen-activated protein kinase 8 Homo sapiens 212-215 22906494-11 2012 The data suggest that the mechanism of menadione-induced JNK activation involves the production of reactive oxygen species, likely superoxide anion, and intracellular GSH levels play an important role in preventing GSTA1-JNK complex dissociation, subsequent JNK activation and induction of cytotoxicity. Superoxides 131-147 mitogen-activated protein kinase 8 Homo sapiens 57-60 24561578-4 2014 Further, oxLDL induced Nox2/superoxide-dependent TRAF3IP2 expression, IKK/p65 and JNK/c-Jun activation, and LOX-1 upregulation, suggesting a reinforcing mechanism. Superoxides 28-38 mitogen-activated protein kinase 8 Homo sapiens 82-85 23417568-4 2013 In the current study, we scrutinized the effects of hydrogen peroxide and/or menadione (superoxide anion generator) on JNK/p38-MAPKs and JAK2-STAT3 pathways to elucidate the mechanism(s) by which each oxidant modulated the above-mentioned pathways leading to SK-N-MC cell death. Superoxides 88-104 mitogen-activated protein kinase 8 Homo sapiens 119-122 23559002-8 2013 Notably, blocking superoxide production attenuated JNK activation as well as cell death induced by simvastatin. Superoxides 18-28 mitogen-activated protein kinase 8 Homo sapiens 51-54 23559002-10 2013 Taken together, our data highlight the critical role of non-canonical regulation of Rho GTPases and involvement of downstream superoxide-mediated activation of JNK pathway in the anticancer activity of simvastatin, which would have potential clinical implications. Superoxides 126-136 mitogen-activated protein kinase 8 Homo sapiens 160-163 23283965-7 2013 Functionally, superoxide flashes in response to hyperosmotic stress participated in the activation of JNK and p38. Superoxides 14-24 mitogen-activated protein kinase 8 Homo sapiens 102-105 22222766-4 2012 The c-Jun N-terminal kinase (JNK) was potently activated after superoxide accumulation. Superoxides 63-73 mitogen-activated protein kinase 8 Homo sapiens 29-32 22222766-5 2012 Suppression of superoxide completely blocked luteolin-induced JNK activation, which was well correlated to alleviation of luteolin"s cytotoxicity. Superoxides 15-25 mitogen-activated protein kinase 8 Homo sapiens 62-65 22222766-7 2012 We further found that luteolin triggers a superoxide-dependent rapid degradation of the JNK-inactivating phosphatase mitogen-activated protein kinase phosphatase-1 (MKP-1). Superoxides 42-52 mitogen-activated protein kinase 8 Homo sapiens 88-91 21635550-6 2011 Additionally, the function of JNK pathway in generation of superoxide anion was determined. Superoxides 59-75 mitogen-activated protein kinase 8 Homo sapiens 30-33 21697181-9 2011 VS cultures treated with JNK inhibitors demonstrated significantly higher levels of MitoSOX Red fluorescence, implying that persistent JNK activity specifically suppresses superoxide production in the mitochondria. Superoxides 172-182 mitogen-activated protein kinase 8 Homo sapiens 25-28 21697181-9 2011 VS cultures treated with JNK inhibitors demonstrated significantly higher levels of MitoSOX Red fluorescence, implying that persistent JNK activity specifically suppresses superoxide production in the mitochondria. Superoxides 172-182 mitogen-activated protein kinase 8 Homo sapiens 135-138 21697181-11 2011 Taken together, these results indicate that persistent JNK activity enhances VS cell survival, at least in part, by suppressing accumulation of mitochondrial superoxides. Superoxides 158-169 mitogen-activated protein kinase 8 Homo sapiens 55-58 21697181-0 2011 Contribution of persistent C-Jun N-terminal kinase activity to the survival of human vestibular schwannoma cells by suppression of accumulation of mitochondrial superoxides. Superoxides 161-172 mitogen-activated protein kinase 8 Homo sapiens 27-50 19846917-9 2009 In addition, the JNK and p38 inhibitors significantly increased the ROS levels including O(2)(-) in the ATO-treated Calu-6 cells. Superoxides 89-93 mitogen-activated protein kinase 8 Homo sapiens 17-20 21454558-7 2011 Mitochondrial superoxide production was shown to be the source of JNK-induced ROS amplification, as an NADPH oxidase inhibitor demonstrated little impact on JNK-mediated ROS generation. Superoxides 14-24 mitogen-activated protein kinase 8 Homo sapiens 66-69 21454558-8 2011 Using mitochondrial isolation from JNK null fibroblasts and targeting the mitochondrial scaffold of JNK, Sab, we demonstrated that mitochondrial JNK signaling was responsible for mitochondrial superoxide amplification. Superoxides 193-203 mitogen-activated protein kinase 8 Homo sapiens 35-38 21454558-8 2011 Using mitochondrial isolation from JNK null fibroblasts and targeting the mitochondrial scaffold of JNK, Sab, we demonstrated that mitochondrial JNK signaling was responsible for mitochondrial superoxide amplification. Superoxides 193-203 mitogen-activated protein kinase 8 Homo sapiens 100-103 21454558-8 2011 Using mitochondrial isolation from JNK null fibroblasts and targeting the mitochondrial scaffold of JNK, Sab, we demonstrated that mitochondrial JNK signaling was responsible for mitochondrial superoxide amplification. Superoxides 193-203 mitogen-activated protein kinase 8 Homo sapiens 100-103 21145826-8 2011 Moreover, menadione or 2,3-dimethoxy-1,4-naphthoquinone, which generate intracellular superoxide anion or hydrogen peroxide, respectively, induced ERK1/2 and JNK1/2 activation and migration. Superoxides 86-102 mitogen-activated protein kinase 8 Homo sapiens 158-162 20139358-6 2010 JNK small interference RNA (siJNK) reduced oxLDL-induced mitochondrial superoxide production by 88.4% and mitochondrial membrane potential by 61.7%. Superoxides 71-81 mitogen-activated protein kinase 8 Homo sapiens 0-3 21460183-5 2011 The increased superoxide content induces c-Jun N-terminal kinase 1 (JNK1) kinase activity, which in turn affects FOXO localization through a compensatory dephosphorylation of Akt. Superoxides 14-24 mitogen-activated protein kinase 8 Homo sapiens 41-66 21460183-5 2011 The increased superoxide content induces c-Jun N-terminal kinase 1 (JNK1) kinase activity, which in turn affects FOXO localization through a compensatory dephosphorylation of Akt. Superoxides 14-24 mitogen-activated protein kinase 8 Homo sapiens 68-72 18206660-9 2008 The results showed that (1) HO-1 is induced in chronic cholestatic liver disease, (2) superoxide anions time- and dose-dependently induce HO-1 activity, (3) HO-1 overexpression inhibits superoxide-anions-induced apoptosis, and (4) CO blocks superoxide-anions-induced JNK phosphorylation and caspase-9, -6, -3 activation and abolishes apoptosis but does not increase necrosis. Superoxides 86-103 mitogen-activated protein kinase 8 Homo sapiens 267-270 18440651-13 2008 In conclusion, IFN-gamma might upregulate ERK, p38, or JNK/ATF-2 phosphorylation induced by GM-CSF or IL-5, leading to enhanced cytokine-induced eosinophil superoxide generation and degranulation. Superoxides 156-166 mitogen-activated protein kinase 8 Homo sapiens 55-58 18206660-9 2008 The results showed that (1) HO-1 is induced in chronic cholestatic liver disease, (2) superoxide anions time- and dose-dependently induce HO-1 activity, (3) HO-1 overexpression inhibits superoxide-anions-induced apoptosis, and (4) CO blocks superoxide-anions-induced JNK phosphorylation and caspase-9, -6, -3 activation and abolishes apoptosis but does not increase necrosis. Superoxides 86-96 mitogen-activated protein kinase 8 Homo sapiens 267-270 18206660-10 2008 We conclude that HO-1 and CO protect primary hepatocytes against superoxide-anions-induced apoptosis partially via inhibition of JNK activity. Superoxides 65-75 mitogen-activated protein kinase 8 Homo sapiens 129-132 16310883-0 2006 Superoxide anions and hydrogen peroxide induce hepatocyte death by different mechanisms: involvement of JNK and ERK MAP kinases. Superoxides 0-17 mitogen-activated protein kinase 8 Homo sapiens 104-107 18439101-9 2008 The JNK inhibitor markedly suppressed TNF-alpha-induced and GM-CSF-induced superoxide release. Superoxides 75-85 mitogen-activated protein kinase 8 Homo sapiens 4-7 18439101-10 2008 These findings suggest that JNK1 and JNK2 are involved in TNF-alpha-induced neutrophil apoptosis and GM-CSF-mediated antiapoptotic effect on neutrophils, respectively, and both JNK isoforms are involved in TNF-alpha-induced and GM-CSF-induced superoxide release. Superoxides 243-253 mitogen-activated protein kinase 8 Homo sapiens 28-32 18439101-10 2008 These findings suggest that JNK1 and JNK2 are involved in TNF-alpha-induced neutrophil apoptosis and GM-CSF-mediated antiapoptotic effect on neutrophils, respectively, and both JNK isoforms are involved in TNF-alpha-induced and GM-CSF-induced superoxide release. Superoxides 243-253 mitogen-activated protein kinase 8 Homo sapiens 28-31 16310883-6 2006 Superoxide anions-induced apoptosis is dependent on JNK activity. Superoxides 0-17 mitogen-activated protein kinase 8 Homo sapiens 52-55 16310883-13 2006 CONCLUSIONS: In normal hepatocytes, superoxide anions-induced caspase activation and apoptosis is dependent on JNK activity and totally abolished by superoxide scavengers. Superoxides 36-53 mitogen-activated protein kinase 8 Homo sapiens 111-114 16310883-13 2006 CONCLUSIONS: In normal hepatocytes, superoxide anions-induced caspase activation and apoptosis is dependent on JNK activity and totally abolished by superoxide scavengers. Superoxides 36-46 mitogen-activated protein kinase 8 Homo sapiens 111-114 11228746-5 1999 TNF-induced JNK activation, similar to NF-kappa B, was inhibited by both superoxide and lipid peroxide quenchers but potentiated by hydroxyl radical quencher. Superoxides 73-83 mitogen-activated protein kinase 8 Homo sapiens 12-15 15993333-7 2005 Under this condition, apoptosis was triggered by an increased production of superoxide that led to a specific activation of the JNK-dependent pathway. Superoxides 76-86 mitogen-activated protein kinase 8 Homo sapiens 128-131 15993333-8 2005 The involvement of superoxide and JNK was demonstrated by cell death inhibition in experiments carried out in the presence of Cu,Zn superoxide dismutase or with specific inhibitors of JNK activity. Superoxides 19-29 mitogen-activated protein kinase 8 Homo sapiens 184-187 15718491-6 2005 In the presence of superoxide scavenger 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), NAD(P)H oxidase inhibitor apocynin, or p38 kinase (an upstream activator of NAD(P)H oxidase) inhibitor SB203850, but not xanthine oxidase inhibitor allopurinol or JNK inhibitor SP600125, the detrimental effect of CRP on serotonin-induced dilation was prevented. Superoxides 19-29 mitogen-activated protein kinase 8 Homo sapiens 260-263 15145937-11 2004 Resistance to death from superoxide therefore requires both PKC/PKD and ERK1/2 activation in order to down-regulate proapoptotic JNK/c-Jun signaling. Superoxides 25-35 mitogen-activated protein kinase 8 Homo sapiens 129-132 15110391-6 2004 Grepafloxacin-induced primed superoxide generation was significantly inhibited by pretreatment with PD169316 and SB203580, p38 mitogen-activated protein kinase (MAPK) inhibitors, but not with PD98059, a specific inhibitor of the upstream kinase that activates p44/42 MAPK, or SP600125, an inhibitor of stress-activated protein kinase/c-Jun N-terminal kinase (JNK). Superoxides 29-39 mitogen-activated protein kinase 8 Homo sapiens 359-362 15569826-10 2005 ANP-evoked production of superoxide was found to activate c-Jun N-terminal kinase (JNK). Superoxides 25-35 mitogen-activated protein kinase 8 Homo sapiens 58-81 15569826-10 2005 ANP-evoked production of superoxide was found to activate c-Jun N-terminal kinase (JNK). Superoxides 25-35 mitogen-activated protein kinase 8 Homo sapiens 83-86 11228746-8 1999 Overall, these results suggest that hydroxyl radicals mediate TNF-induced apoptosis but not activation of NF-kappa B, AP-1, and JNK; superoxide radicals mediate NF-kappa B and JNK activation but potentiate apoptosis; and lipid peroxides are required for all the signals induced by TNF. Superoxides 133-143 mitogen-activated protein kinase 8 Homo sapiens 176-179