PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29627323-4 2018 Here, we show that in the process of activating JNK, aggregation prone hA also activates an upstream apoptosis signal regulating kinase-1 (ASK1) with concomitant decrease in intracellular levels of reduced glutathione. Glutathione 206-217 mitogen-activated protein kinase 8 Homo sapiens 48-51 32996404-0 2022 In silico and in vitro investigations on the protein-protein interactions of glutathione S-transferases with mitogen-activated protein kinase 8 and apoptosis signal-regulating kinase 1. Glutathione 77-88 mitogen-activated protein kinase 8 Homo sapiens 109-143 26716417-7 2016 Pretreatment of cells with the thiol antioxidant glutathione or p38 MAPK/JNK inhibitors before Cd treatment effectively abrogated ROS activation of p38 MAPK/JNK pathways and apoptosis-related proteins. Glutathione 49-60 mitogen-activated protein kinase 8 Homo sapiens 157-160 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. Glutathione 146-157 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. Glutathione 277-280 mitogen-activated protein kinase 8 Homo sapiens 104-107 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. Glutathione 361-364 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. Glutathione 164-167 mitogen-activated protein kinase 8 Homo sapiens 55-58 28585211-11 2017 In "second hit" reduced glutathione levels due to oxidative stress lead to overactivation of c-Jun N-terminal kinase (JNK)/c-Jun signaling that induces cell death in the steatotic liver. Glutathione 24-35 mitogen-activated protein kinase 8 Homo sapiens 93-116 28585211-11 2017 In "second hit" reduced glutathione levels due to oxidative stress lead to overactivation of c-Jun N-terminal kinase (JNK)/c-Jun signaling that induces cell death in the steatotic liver. Glutathione 24-35 mitogen-activated protein kinase 8 Homo sapiens 118-121 28485044-4 2017 When the two compounds were joined by a short PEG linker, the resulting bidentate binder (A82-L-B272) was able to covalently modify JNK1 in the presence of a large molar excess of glutathione (0.5 mm), used to simulate intracellular reducing conditions. Glutathione 180-191 mitogen-activated protein kinase 8 Homo sapiens 132-136 26878775-4 2016 ECG attenuated lipopolysaccharide (LPS)-induced inflammatory mediator expression and intracellular reactive oxygen species (ROS) generation through the induction of Nrf2/antioxidant response element (ARE)-driven glutathione (GSH) and hemeoxygenase-1 (HO-1) levels, interference with NF-kappaB and Nfr2/ARE transcriptional activities, and suppression of the MAPKs (JNK1/2 and p38) and PI3K/Akt signaling pathways. Glutathione 212-223 mitogen-activated protein kinase 8 Homo sapiens 364-370 26235743-10 2015 Pretreatment with the antioxidants N-acetyl cysteine or glutathione attenuated 8m-induced apoptosis and JNK activation in HCT116 cells. Glutathione 56-67 mitogen-activated protein kinase 8 Homo sapiens 104-107 21937211-0 2012 Stimulation of GSH synthesis to prevent oxidative stress-induced apoptosis by hydroxytyrosol in human retinal pigment epithelial cells: activation of Nrf2 and JNK-p62/SQSTM1 pathways. Glutathione 15-18 mitogen-activated protein kinase 8 Homo sapiens 159-162 24997392-9 2014 Inhibiting the ROS production using Nox4 siRNA or antagonizing ROS using GSH reduced cellular ROS level and attenuated AGE-induced GRP78 expression and IRE1alpha and JNK activation. Glutathione 73-76 mitogen-activated protein kinase 8 Homo sapiens 166-169 23660987-6 2013 Both JNK and p38 inhibitors intensified growth inhibition, cell death, MMP ( Psi(m)) loss and GSH depletion by GA. Glutathione 94-97 mitogen-activated protein kinase 8 Homo sapiens 5-8 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. Glutathione 167-170 mitogen-activated protein kinase 8 Homo sapiens 57-60 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. Glutathione 167-170 mitogen-activated protein kinase 8 Homo sapiens 221-224 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. Glutathione 167-170 mitogen-activated protein kinase 8 Homo sapiens 221-224 24040019-0 2013 Synergistic apoptosis of CML cells by buthionine sulfoximine and hydroxychavicol correlates with activation of AIF and GSH-ROS-JNK-ERK-iNOS pathway. Glutathione 119-122 mitogen-activated protein kinase 8 Homo sapiens 127-130 24040019-13 2013 CONCLUSION/SIGNIFICANCE: BSO synergizes with HCH in inducing apoptosis of CML cells through the GSH-ROS-JNK-ERK-iNOS pathway. Glutathione 96-99 mitogen-activated protein kinase 8 Homo sapiens 104-107 22894569-10 2012 These results suggest that the attenuation of 6-OHDA-induced apoptosis by CA is associated with the Nrf2-driven synthesis of GSH, which in turn down-regulates the JNK and p38 signaling pathways. Glutathione 125-128 mitogen-activated protein kinase 8 Homo sapiens 163-166 22246135-5 2012 In addition, our results showed that the exposure of SK-N-MC cells to H(2)O(2) ended up in reduction of glutathione (GSH) levels of SK-N-MC cells via JNK/ERK-mediated down-regulation of gamma-glutamyl-cysteine synthetase (gamma-GCS) expression. Glutathione 104-115 mitogen-activated protein kinase 8 Homo sapiens 150-153 21523454-4 2012 Modulation of (a) intracellular glutathione (GSH) level was done by using L: -buthionine sulfoximine (BSO) or diethylmaleate (DEM), (b) NADPH oxidase by using diphenyleneiodonium (DPI), and (c) MAP kinases by using SB202190 (p38), SP600125 (JNK), and U0126 (ERK) inhibitors. Glutathione 32-43 mitogen-activated protein kinase 8 Homo sapiens 241-244 21523454-4 2012 Modulation of (a) intracellular glutathione (GSH) level was done by using L: -buthionine sulfoximine (BSO) or diethylmaleate (DEM), (b) NADPH oxidase by using diphenyleneiodonium (DPI), and (c) MAP kinases by using SB202190 (p38), SP600125 (JNK), and U0126 (ERK) inhibitors. Glutathione 45-48 mitogen-activated protein kinase 8 Homo sapiens 241-244 22246135-5 2012 In addition, our results showed that the exposure of SK-N-MC cells to H(2)O(2) ended up in reduction of glutathione (GSH) levels of SK-N-MC cells via JNK/ERK-mediated down-regulation of gamma-glutamyl-cysteine synthetase (gamma-GCS) expression. Glutathione 117-120 mitogen-activated protein kinase 8 Homo sapiens 150-153 21283807-4 2011 The sequence of biochemical events after GSH depletion and irradiation included ASK-1 followed by JNK activation which resulted in the triggering of the intrinsic apoptotic pathway through Bax translocation to mitochondria. Glutathione 41-44 mitogen-activated protein kinase 8 Homo sapiens 98-101 22293863-9 2012 In addition, JNK and p38 siRNAs increased ROS levels and GSH depletion in ATO-treated HPF cells. Glutathione 69-72 mitogen-activated protein kinase 8 Homo sapiens 13-16 22293863-11 2012 siRNAs targeting JNK and p38 showing an increase in ROS levels and GSH depletion in ATO-treated HPF cells augmented cell growth inhibition and death. Glutathione 79-82 mitogen-activated protein kinase 8 Homo sapiens 17-20 21166414-8 2011 In relation to ROS and GSH levels, JNK and p38 inhibitors increased ROS levels, and GSH-depleted cell numbers in GA-treated HeLa cells. Glutathione 23-26 mitogen-activated protein kinase 8 Homo sapiens 35-38 21166414-8 2011 In relation to ROS and GSH levels, JNK and p38 inhibitors increased ROS levels, and GSH-depleted cell numbers in GA-treated HeLa cells. Glutathione 84-87 mitogen-activated protein kinase 8 Homo sapiens 35-38 21166414-11 2011 Conclusively, JNK and p38 inhibitors and p38 siRNA enhanced growth inhibition and cell death in GA-treated HeLa cells, which were to some extent related to GSH depletion and ROS levels, especially O(2)( -). Glutathione 156-159 mitogen-activated protein kinase 8 Homo sapiens 14-17 21319226-7 2011 Further results showed that JNK inhibitor SP600125 and 420116 both reversed ANDRO-induced cytotoxicity, and SP600125 also decreased ANDRO-increased intracellular GSH and GCL activity. Glutathione 162-165 mitogen-activated protein kinase 8 Homo sapiens 28-31 21319226-9 2011 Taken together, our results suggest that there is a crosstalk between JNK activation and cellular GSH homeostasis, and ANDRO targets this to induce cytotoxicity in hepatoma cells. Glutathione 98-101 mitogen-activated protein kinase 8 Homo sapiens 70-73 20060865-0 2010 Glutathione depletion causes a JNK and p38MAPK-mediated increase in expression of cystathionine-gamma-lyase and upregulation of the transsulfuration pathway in C6 glioma cells. Glutathione 0-11 mitogen-activated protein kinase 8 Homo sapiens 31-34 21472273-5 2010 JNK inhibitor also somewhat suppressed cell growth inhibition, MMP (Deltapsim) loss and GSH depletion induced by GA, and limited the increase in ROS levels. Glutathione 88-91 mitogen-activated protein kinase 8 Homo sapiens 0-3 20060865-10 2010 It is concluded that glutathione depletion causes a JNK- and p38(MAPK)-mediated increase in expression of cystathionine-gamma-lyase that promotes flux through the transsulfuration pathway to compensate for loss of glutathione in C6 glioma cells. Glutathione 21-32 mitogen-activated protein kinase 8 Homo sapiens 52-55 20060865-10 2010 It is concluded that glutathione depletion causes a JNK- and p38(MAPK)-mediated increase in expression of cystathionine-gamma-lyase that promotes flux through the transsulfuration pathway to compensate for loss of glutathione in C6 glioma cells. Glutathione 214-225 mitogen-activated protein kinase 8 Homo sapiens 52-55 19956548-8 2009 Together these data support the likelihood that GSH inhibits the effect of parthenolide on JNK, NFkappaB and cell death through its direct inhibition of parthenolide"s modulation of exofacial thiols. Glutathione 48-51 mitogen-activated protein kinase 8 Homo sapiens 91-94 20501438-8 2009 GSH depletion led to overactivation of JNK/c-Jun signaling at the level of mitogen-activated protein kinase kinase 4 that induced cell death. Glutathione 0-3 mitogen-activated protein kinase 8 Homo sapiens 39-42 19846917-8 2009 The treatment with MAP kinase kinase (MEK), c-Jun N-terminal kinase (JNK) and p38 inhibitors intensified the cell growth inhibition, cell death, MMP (DeltaPsi(m)) loss, and GSH depletion in the ATO-treated Calu-6 cells. Glutathione 173-176 mitogen-activated protein kinase 8 Homo sapiens 44-67 19846917-8 2009 The treatment with MAP kinase kinase (MEK), c-Jun N-terminal kinase (JNK) and p38 inhibitors intensified the cell growth inhibition, cell death, MMP (DeltaPsi(m)) loss, and GSH depletion in the ATO-treated Calu-6 cells. Glutathione 173-176 mitogen-activated protein kinase 8 Homo sapiens 69-72 17989939-11 2008 Also, reduction in endogenous GSH along with selenite treatment is associated with increased apoptosis, increased expression of p38 and JNK MAPK, decreased Bcl-2 expression, and increase in caspase-3 expression. Glutathione 30-33 mitogen-activated protein kinase 8 Homo sapiens 136-139 18636161-0 2008 The association of deamidation of Bcl-xL and translocation of Bax to the mitochondria through activation of JNK in the induction of apoptosis by treatment with GSH-conjugated DXR. Glutathione 160-163 mitogen-activated protein kinase 8 Homo sapiens 108-111 18636161-12 2008 Therefore, the induction of apoptosis by treatment of HepG2 with GSH-DXR was enhanced, thereby facilitating the release of cytochrome c by both deamidated inactivation of Bcl-xL and functional translocation of Bax to the mitochondria via JNK activation. Glutathione 65-68 mitogen-activated protein kinase 8 Homo sapiens 238-241 19428345-7 2009 Our study showed that esculetin, PD98059 (MEK/ERK inhibitor), and SP600125 (JNK inhibitor) similarly enhanced the As(2)O(3)-induced GSH depletion. Glutathione 132-135 mitogen-activated protein kinase 8 Homo sapiens 76-79 17481858-11 2007 Among various antioxidants used in this study, only thiol-containing antioxidants such as NAC or GSH inhibited both JNK and p38 MAPK activation and apoptosis, indicating the unique protective capacity of thiol compounds. Glutathione 97-100 mitogen-activated protein kinase 8 Homo sapiens 116-119 17920036-0 2007 Regulation of p21Waf1 expression and TNFalpha biosynthesis by glutathione modulators in PMA induced-THP1 differentiation: involvement of JNK and ERK pathways. Glutathione 62-73 mitogen-activated protein kinase 8 Homo sapiens 137-140 17920036-9 2007 Taken together, our findings suggest that the modulation of GSH regulate the magnitude the cell response to PMA in which JNK and ERK have a particular role in redox signaling. Glutathione 60-63 mitogen-activated protein kinase 8 Homo sapiens 121-124 16972261-0 2006 Pharmacologic inhibitors of extracellular signal-regulated kinase (ERKs) and c-Jun NH(2)-terminal kinase (JNK) decrease glutathione content and sensitize human promonocytic leukemia cells to arsenic trioxide-induced apoptosis. Glutathione 120-131 mitogen-activated protein kinase 8 Homo sapiens 106-109 17431793-0 2007 Conformational change in the active center region of GST P1-1, due to binding of a synthetic conjugate of DXR with GSH, enhanced JNK-mediated apoptosis. Glutathione 115-118 mitogen-activated protein kinase 8 Homo sapiens 129-132 17431793-3 2007 In the present experiment, binding of GSH-DXR to GST P1-1 allosterically led to the disappearance of its enzyme activity and activated the kinase activity of JNK without dissociation of the JNK-GST P1-1 complex. Glutathione 38-41 mitogen-activated protein kinase 8 Homo sapiens 158-161 17431793-3 2007 In the present experiment, binding of GSH-DXR to GST P1-1 allosterically led to the disappearance of its enzyme activity and activated the kinase activity of JNK without dissociation of the JNK-GST P1-1 complex. Glutathione 38-41 mitogen-activated protein kinase 8 Homo sapiens 190-193 17431793-8 2007 The findings suggested that allosteric inhibition of GST P1-1 activity by the binding of GSH-DXR following conformational change may activate JNK and induce apoptosis via the mitochondrial pathway in the cells. Glutathione 89-92 mitogen-activated protein kinase 8 Homo sapiens 142-145 16972261-5 2006 Treatment with MEK/ERK and JNK inhibitors, but not with p38 inhibitors, caused intracellular glutathione (GSH) depletion, which was differentially regulated. Glutathione 93-104 mitogen-activated protein kinase 8 Homo sapiens 27-30 16972261-5 2006 Treatment with MEK/ERK and JNK inhibitors, but not with p38 inhibitors, caused intracellular glutathione (GSH) depletion, which was differentially regulated. Glutathione 106-109 mitogen-activated protein kinase 8 Homo sapiens 27-30 17065531-10 2006 dPGJ(2) activated ERK, JNK, and p38; GSH induction by dPGJ(2) depended partially on JNK and p38. Glutathione 37-40 mitogen-activated protein kinase 8 Homo sapiens 84-87 16543941-0 2006 Aplidin induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 phosphatase downregulation. Glutathione 87-98 mitogen-activated protein kinase 8 Homo sapiens 16-19 16543941-4 2006 Exogenous GSH inhibits these effects and also JNK activation and cell death. Glutathione 10-13 mitogen-activated protein kinase 8 Homo sapiens 46-49 16337611-0 2006 Peptide-bond modified glutathione conjugate analogs modulate GSTpi function in GSH-conjugation, drug sensitivity and JNK signaling. Glutathione 22-33 mitogen-activated protein kinase 8 Homo sapiens 117-120 16582599-0 2006 Depletion of intracellular glutathione contributes to JNK-mediated death receptor 5 upregulation and apoptosis induction by the novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me). Glutathione 27-38 mitogen-activated protein kinase 8 Homo sapiens 54-57 16582599-10 2006 These results suggest that depletion of intracellular GSH, but not ROS generation, contributes to CDDO-Me-induced JNK activation and apoptosis, at least in our systems. Glutathione 54-57 mitogen-activated protein kinase 8 Homo sapiens 114-117 16582599-12 2006 Collectively, we conclude that CDDO-Me activates the JNK pathway via depletion of intracellular GSH, leading to DR5 upregulation and induction of apoptosis. Glutathione 96-99 mitogen-activated protein kinase 8 Homo sapiens 53-56 15212948-11 2004 Both UV- and H(2)O(2)-induced JNK activities were inhibited by glutathione, suggesting that the redox status does play an important role in the activation of JNKs. Glutathione 63-74 mitogen-activated protein kinase 8 Homo sapiens 30-33 14701702-4 2004 One mechanism of resistance in these cells is up-regulated glutathione (GSH) content, and GSH depletion by l-buthionine-[S,R]-sulfoximine (BSO) restores JNK activation and As(2)O(3) sensitivity. Glutathione 90-93 mitogen-activated protein kinase 8 Homo sapiens 153-156 14612554-10 2003 SFN was able to activate JNK1/2, and that activation was blocked by treatment with exogenous GSH. Glutathione 93-96 mitogen-activated protein kinase 8 Homo sapiens 25-29 18432922-4 2004 Also described is a procedure for preparing GSThyphen;cJun/GSH-Sepharose beads needed in the solid-phase JNK protein kinase activity assay. Glutathione 59-62 mitogen-activated protein kinase 8 Homo sapiens 105-108 12847227-0 2003 c-Jun N-terminal kinase negatively regulates lipopolysaccharide-induced IL-12 production in human macrophages: role of mitogen-activated protein kinase in glutathione redox regulation of IL-12 production. Glutathione 155-166 mitogen-activated protein kinase 8 Homo sapiens 0-23 12847227-9 2003 Our findings indicate that JNK negatively affects LPS-induced IL-12 production from human macrophages, and that glutathione redox regulates LPS-induced IL-12 production through the opposite control of JNK and p38 MAP kinase activation. Glutathione 112-123 mitogen-activated protein kinase 8 Homo sapiens 201-204 12819184-10 2003 EGCG-induced JNK activation was blocked by the antioxidants glutathione and N-acetyl-l-cysteine, suggesting that the cell death signaling was potentially triggered by oxidative stress. Glutathione 60-71 mitogen-activated protein kinase 8 Homo sapiens 13-16 12847227-2 2003 The present study uses human macrophages to examine whether the JNK pathway is required for LPS-induced IL-12 production and defines how JNK is involved in the regulation of IL-12 production by glutathione redox, which is the balance between intracellular reduced (GSH) and oxidized glutathione (GSSG). Glutathione 194-205 mitogen-activated protein kinase 8 Homo sapiens 137-140 12847227-2 2003 The present study uses human macrophages to examine whether the JNK pathway is required for LPS-induced IL-12 production and defines how JNK is involved in the regulation of IL-12 production by glutathione redox, which is the balance between intracellular reduced (GSH) and oxidized glutathione (GSSG). Glutathione 265-268 mitogen-activated protein kinase 8 Homo sapiens 137-140 12847227-2 2003 The present study uses human macrophages to examine whether the JNK pathway is required for LPS-induced IL-12 production and defines how JNK is involved in the regulation of IL-12 production by glutathione redox, which is the balance between intracellular reduced (GSH) and oxidized glutathione (GSSG). Glutathione 283-294 mitogen-activated protein kinase 8 Homo sapiens 137-140 12847227-8 2003 GSH-OEt augmented p38 MAP kinase activation, but suppressed the JNK activation induced by LPS. Glutathione 0-3 mitogen-activated protein kinase 8 Homo sapiens 64-67 12414812-7 2003 The intracellular level of GSH affected Aplidin action; pretreatment of cells with GSH or N-acetylcysteine inhibited, whereas GSH depletion caused, hyperinduction of EGFR, Src, JNK, and p38 MAPK. Glutathione 83-86 mitogen-activated protein kinase 8 Homo sapiens 177-180 9360968-9 1997 Pretreatment with N-acetyl-L-cysteine, glutathione, or vitamin E attenuated ERK2 but not JNK1 activation by BHA and tBHQ. Glutathione 39-50 mitogen-activated protein kinase 8 Homo sapiens 89-93 12361807-7 2002 These data reveal that de novo GSH biosynthesis in response to 4HNE signals through the JNK pathway and suggests a major role for AP-1 driven expression of both Gcl genes in HBE1 cells. Glutathione 31-34 mitogen-activated protein kinase 8 Homo sapiens 88-91 11768769-7 2001 Free radical scavengers N-acetyl-L-cysteine (NAC), or glutathione (GSH), inhibited ERK2 activation and, to a much lesser extent, JNK1 activation by BHA/tBHQ, implicating the role of oxidative stress. Glutathione 54-65 mitogen-activated protein kinase 8 Homo sapiens 129-133 11279018-4 2001 Raising intracellular ROS by depletion of glutathione with buthionine sulfoximine (BSO) or glutamine starvation resulted in down-regulation of Pgp and p27Kip1, whereas ERK1,2 and JNK were activated. Glutathione 42-53 mitogen-activated protein kinase 8 Homo sapiens 179-182 10873716-5 2000 EC treated with buthionine-sulphoximine (BSO), an inhibitor of glutathione synthesis, further enhanced PCB-induced JNK/SAPK activity. Glutathione 63-74 mitogen-activated protein kinase 8 Homo sapiens 115-118 10873716-7 2000 Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK. Glutathione 31-42 mitogen-activated protein kinase 8 Homo sapiens 100-108 10734112-4 2000 Interestingly, pretreatment with the antioxidants, N-acetyl-L-cysteine, dithiothreitol, and glutathione, impaired chelerythrine-induced JNK1 and p38 activation. Glutathione 92-103 mitogen-activated protein kinase 8 Homo sapiens 136-140 10719239-4 2000 Expression of a catalytically inactive dominant negative JNK1 in MCF-7/ADR inhibited glucose deprivation- induced cell death and the accumulation of oxidized glutathione as well as altered the duration of JNK activation from persistent (> 2 h) to transient (30 min). Glutathione 158-169 mitogen-activated protein kinase 8 Homo sapiens 57-61 10719239-4 2000 Expression of a catalytically inactive dominant negative JNK1 in MCF-7/ADR inhibited glucose deprivation- induced cell death and the accumulation of oxidized glutathione as well as altered the duration of JNK activation from persistent (> 2 h) to transient (30 min). Glutathione 158-169 mitogen-activated protein kinase 8 Homo sapiens 57-60 10719239-6 2000 Finally, a linear dose response suppression of oxidized glutathione accumulation was noted for clones expressing increasing levels of dominant negative JNK1 during glucose deprivation. Glutathione 56-67 mitogen-activated protein kinase 8 Homo sapiens 152-156 12671299-5 1998 Pretreatment with free radical scavengers N-acetyl-L-cysteine (NAC), glutathione (GSH), or vitamin E, inhibited ERK2 activation and, to a much lesser extent, JNK 1 activation by BHA and tBHQ, implicating the role of oxidative stress. Glutathione 69-80 mitogen-activated protein kinase 8 Homo sapiens 158-163 12671299-5 1998 Pretreatment with free radical scavengers N-acetyl-L-cysteine (NAC), glutathione (GSH), or vitamin E, inhibited ERK2 activation and, to a much lesser extent, JNK 1 activation by BHA and tBHQ, implicating the role of oxidative stress. Glutathione 82-85 mitogen-activated protein kinase 8 Homo sapiens 158-163 12414812-7 2003 The intracellular level of GSH affected Aplidin action; pretreatment of cells with GSH or N-acetylcysteine inhibited, whereas GSH depletion caused, hyperinduction of EGFR, Src, JNK, and p38 MAPK. Glutathione 27-30 mitogen-activated protein kinase 8 Homo sapiens 177-180 12414812-7 2003 The intracellular level of GSH affected Aplidin action; pretreatment of cells with GSH or N-acetylcysteine inhibited, whereas GSH depletion caused, hyperinduction of EGFR, Src, JNK, and p38 MAPK. Glutathione 83-86 mitogen-activated protein kinase 8 Homo sapiens 177-180 11522656-6 2001 Expression of dominant negative mutants of ERK1, MAPK/ERK activator-1, or JNK1 but not p38 blocked phosphorylation of the substrate glutathione S-transferase-c-Jun and inhibited VES-induced apoptosis. Glutathione 132-143 mitogen-activated protein kinase 8 Homo sapiens 74-78 11035067-5 2000 Lowering the intracellular GSH/GSH disulfide ratio by BCNU, HP, or NO resulted in all cases in the fulminant enhancement of Jun-N-terminal kinase and p38 mitogen-activated protein kinase but not extracellular signal-regulated kinase 1/2. Glutathione 27-30 mitogen-activated protein kinase 8 Homo sapiens 124-145 10496957-8 1999 Depletion of glutathione reversed NO/O(2)(-)-evoked survival to cell destruction and reinstalled JNK1/2 activity. Glutathione 13-24 mitogen-activated protein kinase 8 Homo sapiens 97-103 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 32-43 mitogen-activated protein kinase 8 Homo sapiens 72-80 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 32-43 mitogen-activated protein kinase 8 Homo sapiens 72-75 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 45-48 mitogen-activated protein kinase 8 Homo sapiens 72-80 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 45-48 mitogen-activated protein kinase 8 Homo sapiens 72-75 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 114-117 mitogen-activated protein kinase 8 Homo sapiens 72-80 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 114-117 mitogen-activated protein kinase 8 Homo sapiens 72-75 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 114-117 mitogen-activated protein kinase 8 Homo sapiens 72-80 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 114-117 mitogen-activated protein kinase 8 Homo sapiens 72-75 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 114-117 mitogen-activated protein kinase 8 Homo sapiens 72-80 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Glutathione 114-117 mitogen-activated protein kinase 8 Homo sapiens 72-75