PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 1 Homo sapiens 112-116 12671299-12 1998 The exact mechanisms by which MAPK and caspases are activated by these agents are currently unknown, but may involve oxidative modification of glutathione (GSH) and/or protein thiols, and/or generation of secondary messengers, ceramide and calcium, which further activate downstream events. Glutathione 143-154 mitogen-activated protein kinase 1 Homo sapiens 30-34 12671299-12 1998 The exact mechanisms by which MAPK and caspases are activated by these agents are currently unknown, but may involve oxidative modification of glutathione (GSH) and/or protein thiols, and/or generation of secondary messengers, ceramide and calcium, which further activate downstream events. Glutathione 156-159 mitogen-activated protein kinase 1 Homo sapiens 30-34 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 1 Homo sapiens 112-116 33684094-12 2021 CONCLUSIONS Selenium and peroxynitrite can influence immune function in imDCs by regulating levels of reactive oxygen species or glutathione to activate ERK and promote antigen phagocytosis, as well as by decreasing MMP2 expression to inhibit chemotactic migration. Glutathione 129-140 mitogen-activated protein kinase 1 Homo sapiens 153-156 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 1 Homo sapiens 76-80 32709140-0 2020 Targeting the MAPK/ERK and PI3K/AKT Signaling Pathways Affects NRF2, Trx and GSH Antioxidant Systems in Leukemia Cells. Glutathione 77-80 mitogen-activated protein kinase 1 Homo sapiens 19-22 32390005-5 2020 The ERK pathway and reactive oxygen species (ROS) played essential roles in mediating Gem+Rom+Cis-induced caspase activation, DNA oxidation and damage, glutathione reduction, and unfolded protein response. Glutathione 152-163 mitogen-activated protein kinase 1 Homo sapiens 4-7 27829272-0 2017 Galangin Activates the ERK/AKT-Driven Nrf2 Signaling Pathway to Increase the Level of Reduced Glutathione in Human Keratinocytes. Glutathione 94-105 mitogen-activated protein kinase 1 Homo sapiens 23-26 29958141-13 2018 Oridonin-induced necroptosis was associated by activated JNK, p38, and ERK in 786-O cells, which were abolished by GSH or NAC treatment. Glutathione 115-118 mitogen-activated protein kinase 1 Homo sapiens 71-74 27829272-6 2017 Our results reveal that galangin protects human keratinocytes by activating ERK/AKT-Nrf2, leading to elevated expression of GSH-synthesizing enzymes. Glutathione 124-127 mitogen-activated protein kinase 1 Homo sapiens 76-79 24111577-8 2014 Furthermore, pretreatment with GSH depletion and antioxidants blocked DFO-induced p38 MAPK, ERK, JNK and nuclear factor-kappaB pathways. Glutathione 31-34 mitogen-activated protein kinase 1 Homo sapiens 86-90 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 1 Homo sapiens 375-378 27941930-8 2016 Furthermore, suppression of ASIC1-mediated generation of reactive oxygen species (ROS) by ROS scavengers, such as glutathione or N-acetyl-cysteine causes a decrease in ERK phosphorylation and degradation of IkappaBalpha. Glutathione 114-125 mitogen-activated protein kinase 1 Homo sapiens 168-171 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 1 Homo sapiens 148-151 25201354-8 2014 Specific ERK inhibitor abolished arsenic-induced NRF2 nuclear translocation and GSH synthesis. Glutathione 80-83 mitogen-activated protein kinase 1 Homo sapiens 9-12 25201354-10 2014 Specific p38 inhibitor attenuated arsenic-enhanced GSH synthesis without changing NRF2 nuclear translocation. Glutathione 51-54 mitogen-activated protein kinase 1 Homo sapiens 9-12 25201354-13 2014 Furthermore, it appears that during chronic arsenic exposure, GSH synthesis is regulated by p38 at least in part independent of NRF2. Glutathione 62-65 mitogen-activated protein kinase 1 Homo sapiens 92-95 24111577-8 2014 Furthermore, pretreatment with GSH depletion and antioxidants blocked DFO-induced p38 MAPK, ERK, JNK and nuclear factor-kappaB pathways. Glutathione 31-34 mitogen-activated protein kinase 1 Homo sapiens 92-95 24307199-6 2014 In addition, 3-BrP caused glutathione-dependent stimulation of p38 mitogen-activated protein kinase (MAPK), mitogen-induced extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK), and protein kinase B (Akt)/mammalian target of rapamycin/p70S6K phosphorylation or activation, as well as rapid LKB-1/AMP kinase (AMPK) activation, which was later followed by Akt-mediated inactivation. Glutathione 26-37 mitogen-activated protein kinase 1 Homo sapiens 101-105 24307199-6 2014 In addition, 3-BrP caused glutathione-dependent stimulation of p38 mitogen-activated protein kinase (MAPK), mitogen-induced extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK), and protein kinase B (Akt)/mammalian target of rapamycin/p70S6K phosphorylation or activation, as well as rapid LKB-1/AMP kinase (AMPK) activation, which was later followed by Akt-mediated inactivation. Glutathione 26-37 mitogen-activated protein kinase 1 Homo sapiens 190-193 23647195-9 2013 These observations indicate that ROS/PKC-alpha, Src/Raf/ERK signaling and cPLA2 are active participants in diethylmaleate/iodoacetate-induced astrocyte death and contribute to a vicious cycle between the depletion of ATP/glutathione and the mobilization of chelatable zinc as critical upstream effectors in initiating cytotoxic cascades. Glutathione 221-232 mitogen-activated protein kinase 1 Homo sapiens 56-59 23837948-8 2013 However, pretreatment of the cells with glutathione reversed the apoptosis induced by SeC and 5-FU and recovered the expression of ERK and AKT inactivation, which revealed the important role of reactive oxygen species in cell apoptosis and regulation of ERK and AKT pathways. Glutathione 40-51 mitogen-activated protein kinase 1 Homo sapiens 131-134 23837948-8 2013 However, pretreatment of the cells with glutathione reversed the apoptosis induced by SeC and 5-FU and recovered the expression of ERK and AKT inactivation, which revealed the important role of reactive oxygen species in cell apoptosis and regulation of ERK and AKT pathways. Glutathione 40-51 mitogen-activated protein kinase 1 Homo sapiens 254-257 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 1 Homo sapiens 108-111 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 1 Homo sapiens 258-261 22508521-7 2012 Embelin treatment resulted in activation of extracellular signal-regulated kinase (ERK)1/2 and ROS accumulation, which correlated with downregulation of antioxidant protein SOD1 and consumption of redox modulator reduced glutathione in the XIAP-overexpressing cells. Glutathione 221-232 mitogen-activated protein kinase 1 Homo sapiens 44-90 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 1 Homo sapiens 258-261 21166414-10 2011 Each MAPK inhibitor and siRNA differentially affected ROS and GSH levels in HeLa control cells. Glutathione 62-65 mitogen-activated protein kinase 1 Homo sapiens 5-9 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 1 Homo sapiens 154-157 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 1 Homo sapiens 154-157 20473523-11 2011 CONCLUSION: Oncogenic H-Ras expression and FK228 treatment synergistically induced the ERK pathway, resulting in differentially increased Nox-1 elevation, ROS production, and GSH depletion, leading to differential caspase activation and cell death in oncogenic H-Ras-expressing J82 versus parental cells. Glutathione 175-178 mitogen-activated protein kinase 1 Homo sapiens 87-90 19276532-0 2008 Regulation of GCL activity and cellular glutathione through inhibition of ERK phosphorylation. Glutathione 40-51 mitogen-activated protein kinase 1 Homo sapiens 74-77 19622586-10 2009 Glutathione supplementation reversed the inhibitory effects of EPOX on ERK, which increases the phosphorylation of Mcl-1 at T(163.) Glutathione 0-11 mitogen-activated protein kinase 1 Homo sapiens 71-74 18048013-3 2008 Our results show that treatment of primary rat neurons with the peroxynitrite donor, SIN-1, leads to decreases in glutathione (GSH) levels and cell viability via a novel extracellular-signal-related kinase (ERK)/c-Myc phosphorylation pathway and a reduction in the nuclear expression of NF-E2-related factor-2 (Nrf2) that down-regulate the expression of glutamate cysteine ligase, the rate limiting enzyme for GSH synthesis. Glutathione 114-125 mitogen-activated protein kinase 1 Homo sapiens 170-205 18048013-3 2008 Our results show that treatment of primary rat neurons with the peroxynitrite donor, SIN-1, leads to decreases in glutathione (GSH) levels and cell viability via a novel extracellular-signal-related kinase (ERK)/c-Myc phosphorylation pathway and a reduction in the nuclear expression of NF-E2-related factor-2 (Nrf2) that down-regulate the expression of glutamate cysteine ligase, the rate limiting enzyme for GSH synthesis. Glutathione 114-125 mitogen-activated protein kinase 1 Homo sapiens 207-210 18048013-3 2008 Our results show that treatment of primary rat neurons with the peroxynitrite donor, SIN-1, leads to decreases in glutathione (GSH) levels and cell viability via a novel extracellular-signal-related kinase (ERK)/c-Myc phosphorylation pathway and a reduction in the nuclear expression of NF-E2-related factor-2 (Nrf2) that down-regulate the expression of glutamate cysteine ligase, the rate limiting enzyme for GSH synthesis. Glutathione 127-130 mitogen-activated protein kinase 1 Homo sapiens 170-205 18048013-3 2008 Our results show that treatment of primary rat neurons with the peroxynitrite donor, SIN-1, leads to decreases in glutathione (GSH) levels and cell viability via a novel extracellular-signal-related kinase (ERK)/c-Myc phosphorylation pathway and a reduction in the nuclear expression of NF-E2-related factor-2 (Nrf2) that down-regulate the expression of glutamate cysteine ligase, the rate limiting enzyme for GSH synthesis. Glutathione 127-130 mitogen-activated protein kinase 1 Homo sapiens 207-210 18048013-3 2008 Our results show that treatment of primary rat neurons with the peroxynitrite donor, SIN-1, leads to decreases in glutathione (GSH) levels and cell viability via a novel extracellular-signal-related kinase (ERK)/c-Myc phosphorylation pathway and a reduction in the nuclear expression of NF-E2-related factor-2 (Nrf2) that down-regulate the expression of glutamate cysteine ligase, the rate limiting enzyme for GSH synthesis. Glutathione 410-413 mitogen-activated protein kinase 1 Homo sapiens 170-205 18048013-3 2008 Our results show that treatment of primary rat neurons with the peroxynitrite donor, SIN-1, leads to decreases in glutathione (GSH) levels and cell viability via a novel extracellular-signal-related kinase (ERK)/c-Myc phosphorylation pathway and a reduction in the nuclear expression of NF-E2-related factor-2 (Nrf2) that down-regulate the expression of glutamate cysteine ligase, the rate limiting enzyme for GSH synthesis. Glutathione 410-413 mitogen-activated protein kinase 1 Homo sapiens 207-210 19276532-4 2008 Genetic inhibition of B-Raf, the upstream of ERK, also resulted in increased GCL activity and GSH level. Glutathione 94-97 mitogen-activated protein kinase 1 Homo sapiens 45-48 19276532-6 2008 Therefore, the findings in the present study suggest that inhibition of B-Raf/MEK/ERK pathway might be a promising physiological approach to up-regulate GCL activity and GSH. Glutathione 170-173 mitogen-activated protein kinase 1 Homo sapiens 82-85 17707924-6 2007 However, preincubation with glutathione prevented ERK, Akt and mTOR phosphorylation caused by treatment with leucine. Glutathione 28-39 mitogen-activated protein kinase 1 Homo sapiens 50-53 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 1 Homo sapiens 129-132 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 1 Homo sapiens 67-71 17761302-3 2007 Glutathione depletion by L-buthionine sulfoximine (BSO) enhanced cisplatin cytotoxicity via increasing production of reactive oxygen species (ROS) and activation of ERK. Glutathione 0-11 mitogen-activated protein kinase 1 Homo sapiens 165-168 17761302-4 2007 In contrast, elevation of glutathione by glutathione ethyl ester (GSHE) decreased cisplatin/BSO cytotoxicity by decreasing ROS production and ERK activation. Glutathione 26-37 mitogen-activated protein kinase 1 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 1 Homo sapiens 19-22 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 1 Homo sapiens 19-22 16972261-7 2006 The MEK/ERK inhibitor also potentiated apoptosis and decreased GSH content in As(2)O(3)-treated NB4 human acute promyelocytic leukemia (APL) cells, but none of these effects were produced by the JNK inhibitor. Glutathione 63-66 mitogen-activated protein kinase 1 Homo sapiens 8-11 14697665-7 2003 In addition, the only transient ERK activation, induced by NO under normal GSH conditions, did not cause ERK-dependent cell death. Glutathione 75-78 mitogen-activated protein kinase 1 Homo sapiens 32-35 16357186-4 2005 This event is most likely due to a peculiar surviving pathway of these cells involving: (a) the formation of mixed disulfides between reduced glutathione (GSH) and protein thiols, (b) a higher and inducible glutathione peroxidase activity, and/or (c) an efficient modulation of the phospho-active levels of the extracellular signal-regulated kinases 1 and 2 (ERK 1/2). Glutathione 142-153 mitogen-activated protein kinase 1 Homo sapiens 311-357 16357186-4 2005 This event is most likely due to a peculiar surviving pathway of these cells involving: (a) the formation of mixed disulfides between reduced glutathione (GSH) and protein thiols, (b) a higher and inducible glutathione peroxidase activity, and/or (c) an efficient modulation of the phospho-active levels of the extracellular signal-regulated kinases 1 and 2 (ERK 1/2). Glutathione 155-158 mitogen-activated protein kinase 1 Homo sapiens 311-357 14610070-5 2004 The addition of N-acetyl-L-cysteine, the PKC inhibitor GF109203X, and the MEK/ERK inhibitors PD98059 and U0126 attenuated both apoptosis induction and GSH decrease, whereas the p38 inhibitor SB203580 and the JNK inhibitor SP600125 were ineffective. Glutathione 151-154 mitogen-activated protein kinase 1 Homo sapiens 78-81 15843040-8 2005 These results suggest that GSH-independent modulation of drug transport is a major mechanism explaining the anti-apoptotic action of MEK/ERK inhibitors in cisplatin-treated myeloid cells. Glutathione 27-30 mitogen-activated protein kinase 1 Homo sapiens 137-140 15530848-5 2004 Pretreatment of osteoclasts with the antioxidants N-acetyl-l-cystein and glutathione reduced RANKL-induced Akt, NF-kappaB, and ERK activation. Glutathione 73-84 mitogen-activated protein kinase 1 Homo sapiens 127-130 12083801-6 2002 On the contrary, the ERK phosphorylation by PPARgamma agonists is inhibited by the MEK inhibitor PD98059, GSH, and permeable SOD mimetic MnTBAP. Glutathione 106-109 mitogen-activated protein kinase 1 Homo sapiens 21-24 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 1 Homo sapiens 83-87 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 67-70 mitogen-activated protein kinase 1 Homo sapiens 83-87 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 1 Homo sapiens 43-46 11532983-10 2001 Replenishment of intracellular glutathione (GSH) with GSH monoethylester abolished ERK activation and reduced the chromosomal instability induced by FAA by 80%. Glutathione 31-42 mitogen-activated protein kinase 1 Homo sapiens 83-86 11532983-10 2001 Replenishment of intracellular glutathione (GSH) with GSH monoethylester abolished ERK activation and reduced the chromosomal instability induced by FAA by 80%. Glutathione 44-47 mitogen-activated protein kinase 1 Homo sapiens 83-86