PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27593219-11 2016 Exposure to H2O2 also significantly increased the phosphorylation of p38, JNK and ERK in the H9c2 cells. Hydrogen Peroxide 12-16 Eph receptor B1 Rattus norvegicus 82-85 29052798-0 2018 Curcumin pretreatment prevents hydrogen peroxide-induced oxidative stress through enhanced mitochondrial function and deactivation of Akt/Erk signaling pathways in rat bone marrow mesenchymal stem cells. Hydrogen Peroxide 31-48 Eph receptor B1 Rattus norvegicus 138-141 29327381-14 2018 3-Methyladenine further increased H2 O2 -induced p-ERK expression. Hydrogen Peroxide 34-39 Eph receptor B1 Rattus norvegicus 51-54 28931335-0 2017 Activation of ERK signalling by Src family kinases (SFKs) in DRG neurons contributes to hydrogen peroxide (H2O2)-induced thermal hyperalgesia. Hydrogen Peroxide 88-105 Eph receptor B1 Rattus norvegicus 14-17 28931335-0 2017 Activation of ERK signalling by Src family kinases (SFKs) in DRG neurons contributes to hydrogen peroxide (H2O2)-induced thermal hyperalgesia. Hydrogen Peroxide 107-111 Eph receptor B1 Rattus norvegicus 14-17 28931335-6 2017 Rapid increase in phosphorylation of extracellular signal regulated kinase (ERK) was observed in neurons of dorsal root ganglia after 20 min of H2O2 (10 micromoles/paw) administration, which gradually returned towards normal level within 24 h, following the pattern of thermal hyperalgesia. Hydrogen Peroxide 144-148 Eph receptor B1 Rattus norvegicus 37-74 28931335-6 2017 Rapid increase in phosphorylation of extracellular signal regulated kinase (ERK) was observed in neurons of dorsal root ganglia after 20 min of H2O2 (10 micromoles/paw) administration, which gradually returned towards normal level within 24 h, following the pattern of thermal hyperalgesia. Hydrogen Peroxide 144-148 Eph receptor B1 Rattus norvegicus 76-79 28931335-9 2017 Intrathecal preadministration of Src family kinases (SFKs) inhibitor (PP1) and MEK inhibitor (PD98059) prevented H2O2 induced augmentation of ERK phosphorylation and thermal hyperalgesia. Hydrogen Peroxide 113-117 Eph receptor B1 Rattus norvegicus 142-145 28609843-12 2017 MCL-1 attenuated H2O2-induced PC-12 cell injury by activating JAK/STAT and ERK/MAPK pathways. Hydrogen Peroxide 17-21 Eph receptor B1 Rattus norvegicus 75-78 27593219-13 2016 It also dose-dependently suppressed the H2O2-induced phosphorylation of JNK and ERK but not that of p38. Hydrogen Peroxide 40-44 Eph receptor B1 Rattus norvegicus 80-83 25792238-8 2016 Hydrogen peroxide also enhanced Elk1 reporter activity, a target of the MEK-extracellular-signal-regulated kinase (ERK) pathway. Hydrogen Peroxide 0-17 Eph receptor B1 Rattus norvegicus 72-113 27409597-7 2016 In addition, CS treatment attenuated the cell injury by H2O2 through the inhibition of phosphorylation of p38 and the extracellular signal-regulated kinase (ERK). Hydrogen Peroxide 56-60 Eph receptor B1 Rattus norvegicus 118-155 27409597-7 2016 In addition, CS treatment attenuated the cell injury by H2O2 through the inhibition of phosphorylation of p38 and the extracellular signal-regulated kinase (ERK). Hydrogen Peroxide 56-60 Eph receptor B1 Rattus norvegicus 157-160 25792238-8 2016 Hydrogen peroxide also enhanced Elk1 reporter activity, a target of the MEK-extracellular-signal-regulated kinase (ERK) pathway. Hydrogen Peroxide 0-17 Eph receptor B1 Rattus norvegicus 115-118 26212730-6 2015 Treatment with H2O2 was also shown to increase Nrf-2 and ERK phosphorylation. Hydrogen Peroxide 15-19 Eph receptor B1 Rattus norvegicus 57-60 25715966-11 2015 Genistein also inhibited H2O2-induced activation of the MAPK-signaling pathway including JNK and ERK. Hydrogen Peroxide 25-29 Eph receptor B1 Rattus norvegicus 97-100 26310779-17 2015 Of note, the increase in the levels of phosphorylated extracellular signal-regulated kinase (ERK) and phosphorylated p38 which occurred in response to exposure to H2O2 was inhibited by treatment with SK. Hydrogen Peroxide 163-167 Eph receptor B1 Rattus norvegicus 54-91 26310779-17 2015 Of note, the increase in the levels of phosphorylated extracellular signal-regulated kinase (ERK) and phosphorylated p38 which occurred in response to exposure to H2O2 was inhibited by treatment with SK. Hydrogen Peroxide 163-167 Eph receptor B1 Rattus norvegicus 93-96 25280787-9 2014 H2O2 at toxic levels activated p38 mitogen-activated protein kinases (MAPK) and p53 pathways and increased DNA double strand breaks (DSBs) in microglia, whereas the rescue exerted by sublytic SNAP against toxic H2O2 occurred via the activation of both Akt and extracellular-signal-regulated kinase (ERK) cascades and decreased DNA DSBs. Hydrogen Peroxide 0-4 Eph receptor B1 Rattus norvegicus 260-297 26550832-0 2015 The Protective Effect of INH2BP, a Novel PARP Inhibitor 5-Iodo-6-Amino-1,2-Benzopyrone, Against Hydrogen Peroxide-Induced Apoptosis Through ERK and p38 MAPK in H9c2 Cells. Hydrogen Peroxide 96-113 Eph receptor B1 Rattus norvegicus 140-143 25881893-10 2015 Hydrogen peroxide enhanced phosphorylation of protein kinases such as Akt, MEK, and ERK in intact astrocytes without injury and stress. Hydrogen Peroxide 0-17 Eph receptor B1 Rattus norvegicus 84-87 25881893-11 2015 A MEK inhibitor, U0126, suppressed not only the H2O2-induced ERK phosphorylation but also cytosolic protein release from rat astrocytes. Hydrogen Peroxide 48-52 Eph receptor B1 Rattus norvegicus 61-64 25280787-9 2014 H2O2 at toxic levels activated p38 mitogen-activated protein kinases (MAPK) and p53 pathways and increased DNA double strand breaks (DSBs) in microglia, whereas the rescue exerted by sublytic SNAP against toxic H2O2 occurred via the activation of both Akt and extracellular-signal-regulated kinase (ERK) cascades and decreased DNA DSBs. Hydrogen Peroxide 0-4 Eph receptor B1 Rattus norvegicus 299-302 25246767-7 2014 F2 not only inhibited H2O2-induced and EGF-induced MEK/ERK activation, but also completely blocked both H2O2-induced and angiotensin II-induced increases in NHE activity, suggesting that F2 directly inhibits MEK/ERK and NHE activation. Hydrogen Peroxide 22-26 Eph receptor B1 Rattus norvegicus 55-58 24628420-6 2014 Aortic banding and hydrogen peroxide/aminotriazole increased the oxidative state of the thoracic aorta that was accompanied by ERK activation and decreased relaxation to insulin, and vice versa, acutely lowered oxidative state by superoxide dismutase/catalase improved relaxation. Hydrogen Peroxide 19-36 Eph receptor B1 Rattus norvegicus 127-130 24815749-13 2014 We propose that the sequestration of PDE4D9 in a specific complex together with AMPK, ERK, MK2 and the H2O2-activatable "switch" kinase allows for its selective multi-site phosphorylation, activation and regulation in mitosis. Hydrogen Peroxide 103-107 Eph receptor B1 Rattus norvegicus 86-89 25246767-2 2014 In this study, we investigated the effects of F2 on the extracellular signal-regulated kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)/Na(+)/H(+) exchanger (NHE)/Na(+)/Ca(2+) exchanger (NCX) signal-transduction pathway involved in H2O2-induced Ca(2+) overload, in order to probe the underlying molecular mechanism by which F2 antagonizes myocardial I/R injury. Hydrogen Peroxide 247-251 Eph receptor B1 Rattus norvegicus 146-149 25246767-3 2014 Acute exposure of rat cardiac myocytes to 100 muM H2O2 increased both NHE and NCX activities, as well as levels of phosphorylated MEK and ERK. Hydrogen Peroxide 50-54 Eph receptor B1 Rattus norvegicus 138-141 25277442-9 2014 Meanwhile, H2O2 stimulated an early autophagy response through the ERK/m-TOR signaling pathway. Hydrogen Peroxide 11-15 Eph receptor B1 Rattus norvegicus 67-70 22890880-0 2012 Selenium protects bone marrow stromal cells against hydrogen peroxide-induced inhibition of osteoblastic differentiation by suppressing oxidative stress and ERK signaling pathway. Hydrogen Peroxide 52-69 Eph receptor B1 Rattus norvegicus 157-160 23727614-5 2013 The conditioned medium prepared from the cells cultured in a fresh medium after the treatment with H2O2 had the FGF-1-like activities, which enhanced cholesterol synthesis, signalings to phosphorylate Akt and ERK, and apoE secretion. Hydrogen Peroxide 99-103 Eph receptor B1 Rattus norvegicus 209-212 22890880-6 2012 In addition, selenite pretreatment also suppressed the activation of extracellular signal-regulated kinase (ERK) induced by H2O2. Hydrogen Peroxide 124-128 Eph receptor B1 Rattus norvegicus 69-106 22890880-6 2012 In addition, selenite pretreatment also suppressed the activation of extracellular signal-regulated kinase (ERK) induced by H2O2. Hydrogen Peroxide 124-128 Eph receptor B1 Rattus norvegicus 108-111 22890880-9 2012 These results showed that selenite protected MSCs against H2O2-induced inhibition of osteoblastic differentiation through inhibiting oxidative stress and ERK activation, which provided, for the first time, the mechanistic explanation for the negative association of selenium status and risk of osteoporosis in terms of bone formation. Hydrogen Peroxide 58-62 Eph receptor B1 Rattus norvegicus 154-157 20629637-4 2010 Results indicated that the MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] inhibitor (PD98059) and 10 muM Sal B remarkably prevented BMSCs from H2O2-induced apoptosis through attenuating caspase-3 activation, which is accompanied by the significant up-regulation of Bcl-2. Hydrogen Peroxide 193-197 Eph receptor B1 Rattus norvegicus 72-75 22144097-0 2012 Ampelopsin inhibits H2O2-induced apoptosis by ERK and Akt signaling pathways and up-regulation of heme oxygenase-1. Hydrogen Peroxide 20-24 Eph receptor B1 Rattus norvegicus 46-49 22144097-7 2012 These results suggest that ampelopsin increases cellular antioxidant defense through activation of the ERK and Akt signaling pathways, which induces HO-1 expression and thereby protects PC12 cells from H2O2-induced apoptosis. Hydrogen Peroxide 202-206 Eph receptor B1 Rattus norvegicus 103-106 21440022-6 2011 U120 (a MAPK(erk) pathway inhibitor; 10muM) attenuated the stimulatory effect of hydrogen peroxide on ANP secretion. Hydrogen Peroxide 81-98 Eph receptor B1 Rattus norvegicus 13-16 19787459-4 2010 According to Western blot analysis, pretreatment with salidroside transiently caused the activation of ERK1/2 pathway; a selective inhibitor of the mitogen-activated protein kinase kinase (MAPKK, MEK) blocked salidroside-activated ERK pathway and thus attenuated the influences of salidroside on H(2)O(2)-induced increase in the level of cleaved caspase-3, a chief executant of apoptosis cascades. Hydrogen Peroxide 296-304 Eph receptor B1 Rattus norvegicus 103-106 20352476-11 2010 Taken together, our results show increased H(2)O(2) levels and cellular redox imbalance associated to a higher p-ERK and AIF immunocontent, which would contribute to a maladaptive hypertrophy phenotype. Hydrogen Peroxide 43-51 Eph receptor B1 Rattus norvegicus 113-116 17074386-2 2007 We report here that exposure of N2a cells or rat hippocampal neurons in culture to 200 microM H2O2 elicited calcium signals, increased ryanodine receptor S-glutathionylation, and enhanced both ERK and CREB phosphorylation. Hydrogen Peroxide 94-98 Eph receptor B1 Rattus norvegicus 193-196 19681663-7 2010 Immunofluorescent experiments revealed H2O2-induced Egr-1 nuclear sequestration to be also ERK- and JNK-dependent. Hydrogen Peroxide 39-43 Eph receptor B1 Rattus norvegicus 91-94 19501068-0 2009 Clozapine protects PC-12 cells from death due to oxidative stress induced by hydrogen peroxide via a cell-type specific mechanism involving inhibition of extracellular signal-regulated kinase phosphorylation. Hydrogen Peroxide 77-94 Eph receptor B1 Rattus norvegicus 154-191 18091994-6 2007 We showed that H(2)O(2) induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a PI3K inhibitor (LY294002) blocked ERK activation caused by H(2)O(2 )and a specific inhibitor of MEK (U0126) protected cells from apoptosis. Hydrogen Peroxide 15-23 Eph receptor B1 Rattus norvegicus 73-76 18091994-6 2007 We showed that H(2)O(2) induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a PI3K inhibitor (LY294002) blocked ERK activation caused by H(2)O(2 )and a specific inhibitor of MEK (U0126) protected cells from apoptosis. Hydrogen Peroxide 15-23 Eph receptor B1 Rattus norvegicus 128-131 18091994-6 2007 We showed that H(2)O(2) induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a PI3K inhibitor (LY294002) blocked ERK activation caused by H(2)O(2 )and a specific inhibitor of MEK (U0126) protected cells from apoptosis. Hydrogen Peroxide 153-162 Eph receptor B1 Rattus norvegicus 73-76 18091994-6 2007 We showed that H(2)O(2) induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a PI3K inhibitor (LY294002) blocked ERK activation caused by H(2)O(2 )and a specific inhibitor of MEK (U0126) protected cells from apoptosis. Hydrogen Peroxide 153-162 Eph receptor B1 Rattus norvegicus 128-131 18091994-7 2007 On the other hand, blockage of the PI3K/Akt pathway abrogated the protective effect conferred by Sal B and potentated H(2)O(2)-induced apoptosis, suggesting that Sal B prevents H(2)O(2)-induced apoptosis predominantly through the PI3K/Akt (upstream of ERK) pathway. Hydrogen Peroxide 177-185 Eph receptor B1 Rattus norvegicus 252-255 18091994-8 2007 SIGNIFICANCE: Our findings provide the first evidence that H(2)O(2) induces rCMECs apoptosis via the PI3K/MEK/ERK pathway and that Sal B protects rCMECs against H(2)O(2)-induced apoptosis through the PI3K/Akt/Raf/MEK/ERK pathway. Hydrogen Peroxide 59-67 Eph receptor B1 Rattus norvegicus 110-113 17669604-7 2007 MnCl(2)-induced a rapid activation of the extracellular signal-regulated kinase (ERK) and p38-MAPK in microglia that appeared to precede the MnCl(2)-induced H(2)O(2) release, suggesting that ERK and p38-MAPK influenced the MnCl(2)-induced H(2)O(2) release in microglia. Hydrogen Peroxide 239-247 Eph receptor B1 Rattus norvegicus 81-84 17164397-12 2007 We conclude that addition of H(2)O(2) inhibited SK channels by stimulating PTK activity, P38, and ERK in the CCD and that H(2)O(2) enhances the internalization of the SK channels. Hydrogen Peroxide 29-37 Eph receptor B1 Rattus norvegicus 98-101 17164397-8 2007 Since H(2)O(2) has also been demonstrated to activate mitogen-activated protein kinase, P38, and ERK (3), we examined the role of P38 and ERK in mediating the effect of H(2)O(2) on SK channels. Hydrogen Peroxide 6-14 Eph receptor B1 Rattus norvegicus 97-100 17184504-0 2006 Time-dependent transition from H(2)O(2)-extracellular signal-regulated kinase- to O(2)-nitric oxide-dependent mechanisms in the stimulatory effect of leptin on renal Na+/K+/-ATPase in the rat. Hydrogen Peroxide 31-39 Eph receptor B1 Rattus norvegicus 40-77 17164397-10 2007 However, combined use of ERK, P38, and PTK inhibitors completely abolished the effect of H(2)O(2) on SK channels. Hydrogen Peroxide 89-97 Eph receptor B1 Rattus norvegicus 25-28 17003231-0 2007 Cyclooxygenase, p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase MAPK, Rho kinase, and Src mediate hydrogen peroxide-induced contraction of rat thoracic aorta and vena cava. Hydrogen Peroxide 133-150 Eph receptor B1 Rattus norvegicus 61-98 17003231-8 2007 Our data suggest that, in rat thoracic aorta and vena cava, a COX-derived metabolite is one important mediator of H2O2 contraction, possibly via rho kinase activation, and that H2O2-induced contraction via p38 and Erk MAPK probably occurs independently of TXA2 receptor activation. Hydrogen Peroxide 177-181 Eph receptor B1 Rattus norvegicus 214-217 16814338-5 2006 The cytotoxicity and phosphorylation of ERK proteins induced by H(2)O(2) were blocked by the ERK inhibitor PD98059. Hydrogen Peroxide 64-72 Eph receptor B1 Rattus norvegicus 40-43 16973240-0 2006 H2O2 and Src-dependent transactivation of the EGF receptor mediates the stimulatory effect of leptin on renal ERK and Na+, K+-ATPase. Hydrogen Peroxide 0-4 Eph receptor B1 Rattus norvegicus 110-113 16814338-5 2006 The cytotoxicity and phosphorylation of ERK proteins induced by H(2)O(2) were blocked by the ERK inhibitor PD98059. Hydrogen Peroxide 64-72 Eph receptor B1 Rattus norvegicus 93-96 16814338-6 2006 Catalase addition prevented H(2)O(2)-induced ROS production, ERKs protein phosphorylation, and cell death, and BE dose-dependently inhibited H(2)O(2)-induced ERK protein phosphorylation in C6 cells. Hydrogen Peroxide 28-36 Eph receptor B1 Rattus norvegicus 61-64 16267404-5 2005 Application of exogenous H2O2 caused increased tyrosine phosphorylation and Grb2 binding to IRS-1 in SK-N-BE(2) cells, while exposure to an H2O2 scavenger (N-acetylcysteine) or to a phophatidylinositol-3 kinase inhibitor (wortmannin), and expression of a dominant negative Rac1, decreased the activation of ERK in insulin-stimulated PC12 cells. Hydrogen Peroxide 25-29 Eph receptor B1 Rattus norvegicus 307-310 16179908-11 2005 Furthermore, JNK and ERK were activated by H2O2 and their specific inhibitors SP600125 (for JNK) and U0126 (for ERK1/2) prevented p21Cip1 expression and blocked cell cycle arrest. Hydrogen Peroxide 43-47 Eph receptor B1 Rattus norvegicus 21-24 15965078-5 2005 These findings demonstrate that NAC blocks the NGF-induced H2O2/ERK signaling in PC12 cells. Hydrogen Peroxide 59-63 Eph receptor B1 Rattus norvegicus 64-67 16184402-11 2005 Trilinolein also decreased ET-1- or H2O2-induced extracellular signal-regulated kinase (ERK) phosphorylation, c-Jun NH2-terminal kinase (JNK) phosphorylation, and activator protein-1 activation. Hydrogen Peroxide 36-40 Eph receptor B1 Rattus norvegicus 49-86 16184402-11 2005 Trilinolein also decreased ET-1- or H2O2-induced extracellular signal-regulated kinase (ERK) phosphorylation, c-Jun NH2-terminal kinase (JNK) phosphorylation, and activator protein-1 activation. Hydrogen Peroxide 36-40 Eph receptor B1 Rattus norvegicus 88-91 15962331-3 2005 Hydrogen peroxide (H(2)O(2)) induced a dose-dependent activation of ERK, which was dependent on MEK activation. Hydrogen Peroxide 0-17 Eph receptor B1 Rattus norvegicus 68-71 15962331-3 2005 Hydrogen peroxide (H(2)O(2)) induced a dose-dependent activation of ERK, which was dependent on MEK activation. Hydrogen Peroxide 19-27 Eph receptor B1 Rattus norvegicus 68-71 15962331-8 2005 Ribosomal S6 kinase (RSK), a cytoplasmic ERK substrate involved in cell survival, was activated and located in the nucleus of H(2)O(2)-exposed hepatocytes. Hydrogen Peroxide 126-134 Eph receptor B1 Rattus norvegicus 41-44 15878161-7 2005 The inductive properties of angiotensin II and H2O2 on ERK phosphorylation and activator protein-1-mediated reporter activity were found reversed with resveratrol and antioxidants such as N-acetyl-cysteine. Hydrogen Peroxide 47-51 Eph receptor B1 Rattus norvegicus 55-58 12124207-4 2002 We have shown that low doses of H(2)O(2) increase NHE-1 activity in an extracellular signal-regulated kinase (ERK)-dependent manner. Hydrogen Peroxide 32-40 Eph receptor B1 Rattus norvegicus 71-108 15078887-2 2004 Exposure of PC-12-D(2)R cells to 200 microm hydrogen peroxide (H(2)O(2)) induces apoptosis in about half of cells after 24 h. After 1-h exposure to 200 microm H(2)O(2), both antiapoptotic extracellular regulated kinase (ERK) phosphorylation and pro-apoptotic Ser-15-p53 phosphorylation are observed. Hydrogen Peroxide 44-61 Eph receptor B1 Rattus norvegicus 188-218 15078887-2 2004 Exposure of PC-12-D(2)R cells to 200 microm hydrogen peroxide (H(2)O(2)) induces apoptosis in about half of cells after 24 h. After 1-h exposure to 200 microm H(2)O(2), both antiapoptotic extracellular regulated kinase (ERK) phosphorylation and pro-apoptotic Ser-15-p53 phosphorylation are observed. Hydrogen Peroxide 44-61 Eph receptor B1 Rattus norvegicus 220-223 15078887-5 2004 Whereas the proportion of cells activating ERK versus p53 at 1 h depended on H(2)O(2) concentration, individual cells showed exclusively either phospho-p53 formation or activation of ERK and egr1 induction. Hydrogen Peroxide 77-85 Eph receptor B1 Rattus norvegicus 43-46 15683716-6 2005 These data indicated that H2O2 negatively regulates iNOS expression through ERK inhibition independently of p38MAPK. Hydrogen Peroxide 26-30 Eph receptor B1 Rattus norvegicus 76-79 15156562-7 2004 H(2)O(2)-induced apoptosis was preceded by rapid activation of all three classes of mitogen-activated protein kinases (MAPKs): ERK, JNK, and p38. Hydrogen Peroxide 0-8 Eph receptor B1 Rattus norvegicus 127-130 12124207-4 2002 We have shown that low doses of H(2)O(2) increase NHE-1 activity in an extracellular signal-regulated kinase (ERK)-dependent manner. Hydrogen Peroxide 32-40 Eph receptor B1 Rattus norvegicus 110-113 11827698-6 2002 H(2)O(2)-induced ERK activation was inhibited not only by PD98059 (10 microM), but also by the non-selective tyrosine kinase inhibitor genistein (3-100 microM), the EGF receptor kinase inhibitor AG1478 (3-300 nM) and the Src family kinase inhibitor PP2 (0.1-10 microM). Hydrogen Peroxide 0-8 Eph receptor B1 Rattus norvegicus 17-20 11958956-4 2002 PBN pretreatment of PC-12 cells, followed by H(2)O(2) stimulation, results in strong and selective activation of the pro-survival ERK pathway. Hydrogen Peroxide 45-53 Eph receptor B1 Rattus norvegicus 130-133 11958956-5 2002 H(2)O(2) induction of ERK activity in PBN-pretreated cells was shown to be dependent on extracellular Ca(+2) influx. Hydrogen Peroxide 0-8 Eph receptor B1 Rattus norvegicus 22-25 11958956-6 2002 Further analysis of the ERK pathway showed that in PBN-pretreated cells, EGF receptor and the adapter protein SHC were phosphorylated in a Ca(+2)-dependent, ligand-independent manner following H(2)O(2) stimulation. Hydrogen Peroxide 193-201 Eph receptor B1 Rattus norvegicus 24-27 11827698-5 2002 ERK and p38 MAPK activities were both increased by 100 microM H(2)O(2) (peak at 6 min); the ERK kinase inhibitor PD98059 (10 microM), but not the p38 MAPK inhibitor SB203580 (1 microM), inhibited the H(2)O(2)-induced increase in DeltaJ(H). Hydrogen Peroxide 62-70 Eph receptor B1 Rattus norvegicus 0-3 11827698-5 2002 ERK and p38 MAPK activities were both increased by 100 microM H(2)O(2) (peak at 6 min); the ERK kinase inhibitor PD98059 (10 microM), but not the p38 MAPK inhibitor SB203580 (1 microM), inhibited the H(2)O(2)-induced increase in DeltaJ(H). Hydrogen Peroxide 62-70 Eph receptor B1 Rattus norvegicus 92-95 11827698-5 2002 ERK and p38 MAPK activities were both increased by 100 microM H(2)O(2) (peak at 6 min); the ERK kinase inhibitor PD98059 (10 microM), but not the p38 MAPK inhibitor SB203580 (1 microM), inhibited the H(2)O(2)-induced increase in DeltaJ(H). Hydrogen Peroxide 200-208 Eph receptor B1 Rattus norvegicus 0-3 11832430-5 2002 The release of arachidonic acid induced by PDGF together with H(2)O(2) was inhibited partially by an inhibitor of ERK or p38 MAP kinase and completely when the two inhibitors were combined; the inhibitory pattern was similar to that for the phosphorylation of cPLA(2). Hydrogen Peroxide 62-70 Eph receptor B1 Rattus norvegicus 114-117 11827698-5 2002 ERK and p38 MAPK activities were both increased by 100 microM H(2)O(2) (peak at 6 min); the ERK kinase inhibitor PD98059 (10 microM), but not the p38 MAPK inhibitor SB203580 (1 microM), inhibited the H(2)O(2)-induced increase in DeltaJ(H). Hydrogen Peroxide 200-208 Eph receptor B1 Rattus norvegicus 92-95 11827698-8 2002 CONCLUSIONS: Our data demonstrate that, in adult rat ventricular myocytes, (i) hydrogen peroxide stimulates sarcolemmal NHE activity, (ii) this response requires activation of ERK and PKC, but not p38 MAPK, (iii) ERK activation occurs through tyrosine kinase-mediated, but PKC-independent, mechanisms Hydrogen Peroxide 79-96 Eph receptor B1 Rattus norvegicus 176-179 11827698-8 2002 CONCLUSIONS: Our data demonstrate that, in adult rat ventricular myocytes, (i) hydrogen peroxide stimulates sarcolemmal NHE activity, (ii) this response requires activation of ERK and PKC, but not p38 MAPK, (iii) ERK activation occurs through tyrosine kinase-mediated, but PKC-independent, mechanisms Hydrogen Peroxide 79-96 Eph receptor B1 Rattus norvegicus 213-216 11522453-8 2001 Nonetheless, as hydrogen peroxide was necessary for ERK activation by ZAS, this indicates that, in contrast to ADP, ZAS stimulates a pathway that is targeted by hydrogen peroxide and leads to ERK activation. Hydrogen Peroxide 16-33 Eph receptor B1 Rattus norvegicus 52-55 11709495-7 2002 First, pharmacologic inhibition of ERK and Akt activation in young cells markedly increased their sensitivity to H2O2. Hydrogen Peroxide 113-117 Eph receptor B1 Rattus norvegicus 35-38 11709495-8 2002 Second, caloric restriction, which increases rodent life span and delays the onset of many age-related declines in physiologic function, prevented loss in ERK and Akt activation by H2O2 and enhanced survival of old hepatocytes to levels similar to those of young cells. Hydrogen Peroxide 181-185 Eph receptor B1 Rattus norvegicus 155-158 11522453-8 2001 Nonetheless, as hydrogen peroxide was necessary for ERK activation by ZAS, this indicates that, in contrast to ADP, ZAS stimulates a pathway that is targeted by hydrogen peroxide and leads to ERK activation. Hydrogen Peroxide 16-33 Eph receptor B1 Rattus norvegicus 192-195 11522453-8 2001 Nonetheless, as hydrogen peroxide was necessary for ERK activation by ZAS, this indicates that, in contrast to ADP, ZAS stimulates a pathway that is targeted by hydrogen peroxide and leads to ERK activation. Hydrogen Peroxide 161-178 Eph receptor B1 Rattus norvegicus 52-55 10629859-3 1999 Treatment of the rat neonatal myocytes with H2O2 resulted in activation of mitogen-activated protein kinases (MAPKs) such as extracellular signal regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK) and p38. Hydrogen Peroxide 44-48 Eph receptor B1 Rattus norvegicus 125-162 11158263-0 2001 Lipid constituents in oligodendroglial cells alter susceptibility to H2O2-induced apoptotic cell death via ERK activation. Hydrogen Peroxide 69-73 Eph receptor B1 Rattus norvegicus 107-110 11158263-4 2001 Exposure of DHA-enriched cells to 0.5 mM H2O2, caused sustained activation of ERK up to 24 h. At this time massive apoptotic cell death was demonstrated by ladder and TUNEL techniques. Hydrogen Peroxide 41-45 Eph receptor B1 Rattus norvegicus 78-81 11158263-5 2001 H2O2-induced stress applied to dEa or DHA/dEa co-supplemented cells showed only a transient ERK activation and no cell death after 24 h. Moreover, while ERK was rapidly translocated into the nucleus in DHA-enriched cells, dEa supplements completely blocked ERK nuclear translocation. Hydrogen Peroxide 0-4 Eph receptor B1 Rattus norvegicus 92-95 11158263-5 2001 H2O2-induced stress applied to dEa or DHA/dEa co-supplemented cells showed only a transient ERK activation and no cell death after 24 h. Moreover, while ERK was rapidly translocated into the nucleus in DHA-enriched cells, dEa supplements completely blocked ERK nuclear translocation. Hydrogen Peroxide 0-4 Eph receptor B1 Rattus norvegicus 153-156 11158263-5 2001 H2O2-induced stress applied to dEa or DHA/dEa co-supplemented cells showed only a transient ERK activation and no cell death after 24 h. Moreover, while ERK was rapidly translocated into the nucleus in DHA-enriched cells, dEa supplements completely blocked ERK nuclear translocation. Hydrogen Peroxide 0-4 Eph receptor B1 Rattus norvegicus 153-156 11158263-6 2001 This study suggests that H2O2-induced apoptotic cell death is associated with prolonged ERK activation and nuclear translocation in DHA-enriched OLN 93 cells, while both phenomena are prevented by dEa supplements. Hydrogen Peroxide 25-29 Eph receptor B1 Rattus norvegicus 88-91 11100733-5 2000 Here we show that inhibition of the betagamma-subunit of G protein (G betagamma) attenuates hydrogen peroxide (H2O2)-induced ERK activation in rat neonatal cardiomyocytes. Hydrogen Peroxide 92-109 Eph receptor B1 Rattus norvegicus 125-128 11100733-5 2000 Here we show that inhibition of the betagamma-subunit of G protein (G betagamma) attenuates hydrogen peroxide (H2O2)-induced ERK activation in rat neonatal cardiomyocytes. Hydrogen Peroxide 111-115 Eph receptor B1 Rattus norvegicus 125-128 11100733-6 2000 The G betagamma-responsive ERK activation induced by H2O2 is independent of ligands binding to Gi-coupled receptors, but requires phosphatidylinositol-3-kinase and Src activation. Hydrogen Peroxide 53-57 Eph receptor B1 Rattus norvegicus 27-30 10801894-4 2000 Activation of ERK by ONOO(-) and H(2)O(2) was blocked by the antioxidant N-acetyl-l-cysteine. Hydrogen Peroxide 33-41 Eph receptor B1 Rattus norvegicus 14-17 10801894-5 2000 Catalase blocked ERK activation by H(2)O(2), but not by ONOO(-), demonstrating that the effect of ONOO(-) was not due to the generation of H(2)O(2). Hydrogen Peroxide 35-43 Eph receptor B1 Rattus norvegicus 17-20 10801894-7 2000 However, the EGFR tyrosine kinase inhibitor AG1478 abolished ERK activation by H(2)O(2), but not by ONOO(-). Hydrogen Peroxide 79-87 Eph receptor B1 Rattus norvegicus 61-64 10801894-9 2000 However, the Raf inhibitor forskolin blocked ERK activation by H(2)O(2), but not by ONOO(-). Hydrogen Peroxide 63-71 Eph receptor B1 Rattus norvegicus 45-48 10801894-10 2000 The MEK inhibitor PD98059 inhibited ERK activation by both H(2)O(2) and ONOO(-). Hydrogen Peroxide 59-67 Eph receptor B1 Rattus norvegicus 36-39 10801894-15 2000 In contrast, H(2)O(2)-induced ERK activation is dependent on EGFR activation, which then leads to downstream Raf-1 and MEK-1 activation. Hydrogen Peroxide 13-21 Eph receptor B1 Rattus norvegicus 30-33 11440832-5 2001 Activation of extracellular signal-regulated protein kinase (ERK) by H2O2 was blunted by AG1478. Hydrogen Peroxide 69-73 Eph receptor B1 Rattus norvegicus 14-59 11440832-5 2001 Activation of extracellular signal-regulated protein kinase (ERK) by H2O2 was blunted by AG1478. Hydrogen Peroxide 69-73 Eph receptor B1 Rattus norvegicus 61-64 11440832-6 2001 PD98059, a specific inhibitor of ERK kinase (MEK1), reduced H2O2-induced AR expression. Hydrogen Peroxide 60-64 Eph receptor B1 Rattus norvegicus 33-36 11231909-5 2001 Inhibition of JAK2 activity with AG-490 partially inhibited H(2)O(2)-induced ERK2 activity, suggesting that JAK2 is upstream of the Ras/Raf/mitogen-activated protein kinase-ERK/ERK mitogenic pathway. Hydrogen Peroxide 60-68 Eph receptor B1 Rattus norvegicus 77-80 11231909-5 2001 Inhibition of JAK2 activity with AG-490 partially inhibited H(2)O(2)-induced ERK2 activity, suggesting that JAK2 is upstream of the Ras/Raf/mitogen-activated protein kinase-ERK/ERK mitogenic pathway. Hydrogen Peroxide 60-68 Eph receptor B1 Rattus norvegicus 173-176 11033117-6 2000 In contrast, FCS inhibited H(2)O(2)-induced apoptosis via the Akt and also the ERK pathway. Hydrogen Peroxide 27-35 Eph receptor B1 Rattus norvegicus 79-82 10861219-5 2000 ERK activation by H(2)O(2), but not phorbol esters, was also sensitive to mitochondrial inhibition. Hydrogen Peroxide 18-26 Eph receptor B1 Rattus norvegicus 0-3 10861219-6 2000 Thus, reoxygenation and H(2)O(2)-mediated oxidative stress share a mechanism of ERK activation that is ATP- or mitochondrion-dependent, and this common feature suggests that the reoxygenation response is mediated by reactive oxygen species. Hydrogen Peroxide 24-32 Eph receptor B1 Rattus norvegicus 80-83 10629859-3 1999 Treatment of the rat neonatal myocytes with H2O2 resulted in activation of mitogen-activated protein kinases (MAPKs) such as extracellular signal regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK) and p38. Hydrogen Peroxide 44-48 Eph receptor B1 Rattus norvegicus 164-167 10629859-5 1999 Expression of GRK2-ct inhibited the H2O2-induced activation of ERK by 70% and also inhibited the activation of Akt by 30%. Hydrogen Peroxide 36-40 Eph receptor B1 Rattus norvegicus 63-66 10629859-6 1999 In contrast with H2O2-induced activation of ERK, the activation of ERK induced by phorbol ester PMA and the activation of JNK and p38 induced by H2O2 were not affected by expression of GRK2-ct, indicating that the activation of ERK but not JNK and p38 is dependent on beta gamma subunit. Hydrogen Peroxide 17-21 Eph receptor B1 Rattus norvegicus 44-47 10629859-7 1999 Among several inhibitors for analyzing intracellular signaling pathways, wortmannin inhibited the activation of ERK by H2O2 treatment. Hydrogen Peroxide 119-123 Eph receptor B1 Rattus norvegicus 112-115 10629859-8 1999 These data suggest that treatment of the rat neonatal myocytes with H2O2 releases beta gamma subunit from heterotrimeric G protein, and leads to activation of ERK in part by phosphatidylinositol-3 kinase dependent pathway. Hydrogen Peroxide 68-72 Eph receptor B1 Rattus norvegicus 159-162 9769235-4 1998 In contrast, higher concentrations of menadione or H 2O2 caused less DNA fragmentation, more necrotic cell death and preferential activation of the extracellular signal-regulated kinase (ERK) pathway. Hydrogen Peroxide 51-56 Eph receptor B1 Rattus norvegicus 148-185 10356288-9 1999 These data show that, in ZAS-stimulated rat AM, activation of the respiratory burst and production of hydrogen peroxide via superoxide dismutation are largely responsible for the activation of the ERK pathway through an upstream target. Hydrogen Peroxide 102-119 Eph receptor B1 Rattus norvegicus 197-200 9886061-0 1999 Hydrogen peroxide activation of multiple mitogen-activated protein kinases in an oligodendrocyte cell line: role of extracellular signal-regulated kinase in hydrogen peroxide-induced cell death. Hydrogen Peroxide 157-174 Eph receptor B1 Rattus norvegicus 116-153 9886061-3 1999 Exposure of CG4 cells to hydrogen peroxide (H2O2) resulted in an increased tyrosine phosphorylation of several protein species, including the abundantly expressed platelet-derived growth factor (PDGF) receptor and the activation of the three MAPK subgroups, i.e., extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK). Hydrogen Peroxide 25-42 Eph receptor B1 Rattus norvegicus 264-301 9886061-3 1999 Exposure of CG4 cells to hydrogen peroxide (H2O2) resulted in an increased tyrosine phosphorylation of several protein species, including the abundantly expressed platelet-derived growth factor (PDGF) receptor and the activation of the three MAPK subgroups, i.e., extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK). Hydrogen Peroxide 25-42 Eph receptor B1 Rattus norvegicus 303-306 9886061-3 1999 Exposure of CG4 cells to hydrogen peroxide (H2O2) resulted in an increased tyrosine phosphorylation of several protein species, including the abundantly expressed platelet-derived growth factor (PDGF) receptor and the activation of the three MAPK subgroups, i.e., extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK). Hydrogen Peroxide 44-48 Eph receptor B1 Rattus norvegicus 264-301 9886061-3 1999 Exposure of CG4 cells to hydrogen peroxide (H2O2) resulted in an increased tyrosine phosphorylation of several protein species, including the abundantly expressed platelet-derived growth factor (PDGF) receptor and the activation of the three MAPK subgroups, i.e., extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK). Hydrogen Peroxide 44-48 Eph receptor B1 Rattus norvegicus 303-306 9769235-4 1998 In contrast, higher concentrations of menadione or H 2O2 caused less DNA fragmentation, more necrotic cell death and preferential activation of the extracellular signal-regulated kinase (ERK) pathway. Hydrogen Peroxide 51-56 Eph receptor B1 Rattus norvegicus 187-190 9374731-2 1997 Here, we demonstrate in rat pleural mesothelial cells that apoptotic concentrations of crocidolite asbestos and H2O2 induce phosphorylation and activation of extracellular signal-regulated protein kinases (ERK). Hydrogen Peroxide 112-116 Eph receptor B1 Rattus norvegicus 158-204 9677316-4 1998 The activation of ERKs by H2O2 was inhibited by PD98059, which inhibits the activation of MAPK (or ERK) kinases, and by the protein kinase C (PKC) inhibitor, GF109203X. Hydrogen Peroxide 26-30 Eph receptor B1 Rattus norvegicus 18-21 9374731-2 1997 Here, we demonstrate in rat pleural mesothelial cells that apoptotic concentrations of crocidolite asbestos and H2O2 induce phosphorylation and activation of extracellular signal-regulated protein kinases (ERK). Hydrogen Peroxide 112-116 Eph receptor B1 Rattus norvegicus 206-209 9374731-0 1997 Role of extracellular signal-regulated protein kinases in apoptosis by asbestos and H2O2. Hydrogen Peroxide 84-88 Eph receptor B1 Rattus norvegicus 8-54 9374731-5 1997 Both H2O2- and asbestos-induced activation of ERK was abolished by catalase. Hydrogen Peroxide 5-9 Eph receptor B1 Rattus norvegicus 46-49 8626753-12 1996 Taken together, these studies provide insight into mechanisms of MAPK regulation by H2O2 and suggest that ERK plays a critical role in cell survival following oxidant injury. Hydrogen Peroxide 84-88 Eph receptor B1 Rattus norvegicus 106-109 34474350-0 2021 Shenxiong glucose injection inhibits H2O2-induced H9c2 cell apoptosis by activating the ERK signaling pathway. Hydrogen Peroxide 37-41 Eph receptor B1 Rattus norvegicus 88-91 34474350-10 2021 CONCLUSION: SGI antagonizes H2O2-induced cell apoptosis by activating the ERK pathway. Hydrogen Peroxide 28-32 Eph receptor B1 Rattus norvegicus 74-77 30615921-0 2019 Shengmai injection alleviates H2O2-induced oxidative stress through activation of AKT and inhibition of ERK pathways in neonatal rat cardiomyocytes. Hydrogen Peroxide 30-34 Eph receptor B1 Rattus norvegicus 104-107 35496304-8 2022 The phosphorylation of ERK, JNK, and p38 was attenuated by MA in IRI-induced kidney injury and H2O2-stimulated NRK52 cells. Hydrogen Peroxide 95-99 Eph receptor B1 Rattus norvegicus 23-26 33326961-14 2021 CONCLUSION: CTS protects cardiomyocytes against the H2O2-induced cellular injuries through ERK and NF-kappaB inactivation and ROS scavenging. Hydrogen Peroxide 52-56 Eph receptor B1 Rattus norvegicus 91-94 33379243-7 2020 In addition, FA attenuates the cell injury by H2O2 through the inhibition of phosphorylation of the extracellular signal-regulated kinase (ERK). Hydrogen Peroxide 46-50 Eph receptor B1 Rattus norvegicus 100-137 33379243-7 2020 In addition, FA attenuates the cell injury by H2O2 through the inhibition of phosphorylation of the extracellular signal-regulated kinase (ERK). Hydrogen Peroxide 46-50 Eph receptor B1 Rattus norvegicus 139-142 31358027-6 2019 H2O2 also induced a sudden and the highest level of autophagy at 1 h, and gradually increased apoptosis through ERK pathway. Hydrogen Peroxide 0-4 Eph receptor B1 Rattus norvegicus 112-115 31358027-10 2019 CONCLUSIONS: TGF-beta1 reduced autophagy and apoptosis induced by exogenous H2O2 through downregulating the expression of ERK in AF cells. Hydrogen Peroxide 76-80 Eph receptor B1 Rattus norvegicus 122-125 30896883-0 2019 Activation of the ERK/Creb/Bcl-2 pathway protects periodontal ligament stem cells against hydrogen peroxide-induced oxidative stress. Hydrogen Peroxide 90-107 Eph receptor B1 Rattus norvegicus 18-21 30060293-7 2018 The results showed that pretreatment of taurine could reverse the inhibition of cell viability and suppress the induced apoptosis in a dose-dependent manner: taurine significantly reduced H2O2-induced oxidative damage and expression of CHOP, while it induced protein expression of Nrf2 and beta-catenin and activated ERK phosphorylation. Hydrogen Peroxide 188-192 Eph receptor B1 Rattus norvegicus 317-320 30060293-9 2018 Activation of ERK signaling mediated by taurine in the presence of H2O2 was significantly inhibited by DKK1. Hydrogen Peroxide 67-71 Eph receptor B1 Rattus norvegicus 14-17 28605990-13 2018 CONCLUSIONS: miR-25 protects PC-12 cells against H2O2-induced oxidative damage though regulation of Nrf2 and activation of Wnt/beta-catenin and PI3 K/AKT/ERK signaling. Hydrogen Peroxide 49-53 Eph receptor B1 Rattus norvegicus 154-157