PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18057711-5 2007 Our results suggest that OR-heparin releases high glucose-arrested cells on G(1) phase and inhibits high glucose-induced mesangial cell proliferation through blocking ERK1/2 phosphorylation and delaying S phase progression, which may be in correlation with OR-heparin suppressing ROS accumulation. Reactive Oxygen Species 280-283 mitogen-activated protein kinase 3 Homo sapiens 167-173 17604276-5 2007 By silencing Akt and blocking Erk1/2 MAPK pathways, we also demonstrate that these signals are downstream to Rac-1/reactive oxygen species production and epidermal growth factor receptor activation. Reactive Oxygen Species 115-138 mitogen-activated protein kinase 3 Homo sapiens 30-36 17503468-0 2007 Endosulfan decreases cell growth and apoptosis in human HaCaT keratinocytes: partial ROS-dependent ERK1/2 mechanism. Reactive Oxygen Species 85-88 mitogen-activated protein kinase 3 Homo sapiens 99-105 17503468-10 2007 Taken together, these findings strongly support that endosulfan induces ROS generation leading to sustained ERK1/2 phosphorylation and decrease in cell growth. Reactive Oxygen Species 72-75 mitogen-activated protein kinase 3 Homo sapiens 108-114 17566077-7 2007 Accordingly, p38 and ERK1/2, two MAP kinases downstream of reactive oxygen species, were activated in stable transmembrane-spanning precursor (tm) TNF-expressing cells and were refractory to activation with soluble TNF or VEGF. Reactive Oxygen Species 59-82 mitogen-activated protein kinase 3 Homo sapiens 21-27 17823205-6 2007 Supporting the notion of ROS-mediated NHE-1 activation, stretch increased the ERK1/2 and p90rsk kinases phosphorylation, effect that was cancelled by losartan. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 3 Homo sapiens 78-84 17604276-5 2007 By silencing Akt and blocking Erk1/2 MAPK pathways, we also demonstrate that these signals are downstream to Rac-1/reactive oxygen species production and epidermal growth factor receptor activation. Reactive Oxygen Species 115-138 mitogen-activated protein kinase 3 Homo sapiens 37-41 17958324-0 2007 Reactive oxygen species mediate ET-1-induced activation of ERK1/2 signaling in cultured feline esophageal smooth muscle cells. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 3 Homo sapiens 59-65 17596522-11 2007 These observations suggest that Aldo induces EMT via MR-mediated, mitochondrial-originated, ROS-dependent ERK1/2 activation in renal tubular epithelial cells. Reactive Oxygen Species 92-95 mitogen-activated protein kinase 3 Homo sapiens 106-112 17958324-2 2007 We investigated a possible role for ROS generation in mediating the action of ET-1 on activation of ERK1/2 in cultured feline esophageal smooth muscle cells (ESMC). Reactive Oxygen Species 36-39 mitogen-activated protein kinase 3 Homo sapiens 100-106 17958324-8 2007 Pretreatment of ESMC with N-acetylcysteine, a ROS scavenger, also attenuated the ET-1-induced ERK1/2 activation. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 3 Homo sapiens 94-100 17958324-10 2007 The results suggest that ROS might be critical mediators of the ET-1-induced ERK1/2 signaling events in ESMC. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 3 Homo sapiens 77-83 17494630-8 2007 These pathways, which may be activated simultaneously or selectively, elevate [Ca(2+)](i), activate Src and the ERK1/2 kinase pathways, and activate phosphoinositide 3-kinase and protein kinase B (Akt), NF-kappaB, and reactive oxygen species. Reactive Oxygen Species 218-241 mitogen-activated protein kinase 3 Homo sapiens 112-118 17428837-7 2007 The stimulation of NADPH oxidase-dependent ROS by uric acid resulted in activation of MAP kinases p38 and ERK1/2, a decrease in nitric oxide bioavailability, and an increase in protein nitrosylation and lipid oxidation. Reactive Oxygen Species 43-46 mitogen-activated protein kinase 3 Homo sapiens 106-112 17309078-0 2007 Protein kinase C-ERK1/2 signal pathway switches glucose depletion-induced necrosis to apoptosis by regulating superoxide dismutases and suppressing reactive oxygen species production in A549 lung cancer cells. Reactive Oxygen Species 148-171 mitogen-activated protein kinase 3 Homo sapiens 17-23 17623008-5 2007 This study provides evidence that radio waves induce ERK1/2 activation downstream of the EGF (epidermal growth factor) receptor, which is in turn activated by the release of reactive oxygen species. Reactive Oxygen Species 174-197 mitogen-activated protein kinase 3 Homo sapiens 53-59 17309078-8 2007 We demonstrate that protein kinase C-dependent extracellular regulated kinase 1/2 (ERK1/2) activation also switched GD-induced necrosis to apoptosis through inhibition of ROS production possibly by inducing manganese superoxide dismutase (SOD) expression and by preventing GD-induced degradation of copper zinc SOD. Reactive Oxygen Species 171-174 mitogen-activated protein kinase 3 Homo sapiens 83-89 17460567-10 2007 CONCLUSION: The results suggest that chilling of renal epithelial cells induces ROS generation by NADPH oxidase, which leads to rapid activation of the MEK-ERK1/2 cascade and initiation of cell injury. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 3 Homo sapiens 156-162 17131377-6 2007 Interestingly, ICAM-1 expression in response to TPA-induced PKC activation was linked to the generation of reactive oxygen species (ROS), as pretreatment with NAC (an ROS scavenger) blocked both ErK1/2 activation and ICAM-1 expression induced by TPA. Reactive Oxygen Species 107-130 mitogen-activated protein kinase 3 Homo sapiens 195-201 17205976-10 2007 The ROS formation was inhibited by the extracellular signal-regulated protein kinase (ERK) inhibitor U0126 (10 microM), the tyrosine kinase inhibitor erbstatin-A (25 microM), eliminating calcium from the buffer and by the superoxide dismutase inhibitor diethyldithio-carbamic acid (DDC, 100 microM). Reactive Oxygen Species 4-7 mitogen-activated protein kinase 3 Homo sapiens 86-89 17131377-6 2007 Interestingly, ICAM-1 expression in response to TPA-induced PKC activation was linked to the generation of reactive oxygen species (ROS), as pretreatment with NAC (an ROS scavenger) blocked both ErK1/2 activation and ICAM-1 expression induced by TPA. Reactive Oxygen Species 132-135 mitogen-activated protein kinase 3 Homo sapiens 195-201 17131377-6 2007 Interestingly, ICAM-1 expression in response to TPA-induced PKC activation was linked to the generation of reactive oxygen species (ROS), as pretreatment with NAC (an ROS scavenger) blocked both ErK1/2 activation and ICAM-1 expression induced by TPA. Reactive Oxygen Species 167-170 mitogen-activated protein kinase 3 Homo sapiens 195-201 17132626-4 2007 We show that treatment of macrophages with ATP results in production of reactive oxygen species (ROS), which stimulate the phosphatidylinositol 3-kinase (PI3K) pathway and subsequent Akt and ERK1/2 activation. Reactive Oxygen Species 72-95 mitogen-activated protein kinase 3 Homo sapiens 191-197 17363476-3 2007 Radiation causes a rapid reactive oxygen species-dependent activation of ERBB family and other tyrosine kinases, leading to activation of RAS proteins and multiple protective downstream signaling pathways (e.g., AKT and ERK1/2), which alter transcription factor function and the apoptotic threshold of cells. Reactive Oxygen Species 25-48 mitogen-activated protein kinase 3 Homo sapiens 220-226 17132626-4 2007 We show that treatment of macrophages with ATP results in production of reactive oxygen species (ROS), which stimulate the phosphatidylinositol 3-kinase (PI3K) pathway and subsequent Akt and ERK1/2 activation. Reactive Oxygen Species 97-100 mitogen-activated protein kinase 3 Homo sapiens 191-197 17196568-7 2007 Hypoxia-induced translocation of ERK1/2 and endothelial cell proliferation were also prevented when NAD(P)H oxidase or PARP were inhibited; however, hypoxic ROS formation was not affected in the presence of PARP inhibitor. Reactive Oxygen Species 157-160 mitogen-activated protein kinase 3 Homo sapiens 33-39 16510265-0 2006 Retinol induces the ERK1/2-dependent phosphorylation of CREB through a pathway involving the generation of reactive oxygen species in cultured Sertoli cells. Reactive Oxygen Species 107-130 mitogen-activated protein kinase 3 Homo sapiens 20-26 17308059-10 2007 ROS-quenching agents, inhibition of mitochondrial function, expression of dominant-negative thioredoxin reductase, or expression of dominant-negative apoptosis signaling kinase 1 suppressed JNK1/2 and p38 MAPK activation and reduced cell killing after 17AAG and DCA exposure. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 205-209 17090621-7 2007 The ERK1/2 signaling pathway inhibitor, U0126, also significantly decreased the levels of ROS associated with PAT treatment. Reactive Oxygen Species 90-93 mitogen-activated protein kinase 3 Homo sapiens 4-10 17090621-9 2007 Activation of ERK1/2 signaling pathway is correlated with PAT-mediated ROS. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 3 Homo sapiens 14-20 17007989-5 2006 The spin-trap s-PBN, the ERK1/2 inhibitor U0126 and the antioxidant Vitamin E inhibited the 2-CPA-induced ROS formation completely, while the mitochondrial transition permeability pore blocker cyclosporine A inhibited the ROS formation partly. Reactive Oxygen Species 106-109 mitogen-activated protein kinase 3 Homo sapiens 25-31 17034354-4 2006 The authors review the principal growth-promoting intracellular signaling pathways that are activated by ROS in cardiac myocytes, namely the mitogen-activated protein kinase cascades (extracellular signal-regulated kinases 1/2, c-Jun N-terminal kinases, and p38-mitogen-activated protein kinases) and the phosphoinositide 3-kinase/protein kinase B (Akt) pathway. Reactive Oxygen Species 105-108 mitogen-activated protein kinase 3 Homo sapiens 184-226 16081426-0 2005 Platelet-derived growth factor and reactive oxygen species (ROS) regulate Ras protein levels in primary human fibroblasts via ERK1/2. Reactive Oxygen Species 35-58 mitogen-activated protein kinase 3 Homo sapiens 126-132 16720733-10 2006 Together, these results suggest that IL-10 inhibits GM-CSF-induced priming of ROS production by inhibiting p47PHOX phosphorylation through a decrease in ERK1/2 activity. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 3 Homo sapiens 153-159 16227320-8 2006 HPASMC activation of the MAP kinases ERK1/2 was reduced by the NAD(P)H oxidase inhibitors DPI and 4-(2-aminoethyl)benzenesulfonyl fluoride, suggesting that TGF-beta1 may facilitate proliferation by upregulating Nox4 and ROS production, with transient oxidative inactivation of phosphatases and augmentation of growth signaling cascades. Reactive Oxygen Species 220-223 mitogen-activated protein kinase 3 Homo sapiens 37-43 16234311-15 2006 These data demonstrate that high glucose stimulates GEC hypertrophy through a ROS-dependent activation of ERK1/2 and Akt/PKB. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 3 Homo sapiens 106-112 16984397-6 2006 Moreover, Rac activation induced the generation of reactive oxygen species and subsequent reactive oxygen species-dependent activation of extracellular signal-regulated kinase 1,2. Reactive Oxygen Species 51-74 mitogen-activated protein kinase 3 Homo sapiens 138-179 16984397-6 2006 Moreover, Rac activation induced the generation of reactive oxygen species and subsequent reactive oxygen species-dependent activation of extracellular signal-regulated kinase 1,2. Reactive Oxygen Species 90-113 mitogen-activated protein kinase 3 Homo sapiens 138-179 16984397-9 2006 In conclusion, Rac-induced transcriptional upregulation of tissue inhibitor of metalloproteinase-1 is mediated by reactive oxygen species-dependent activation of extracellular signal-related kinase-1,2 and by transcription factors of the activating protein-1 family. Reactive Oxygen Species 114-137 mitogen-activated protein kinase 3 Homo sapiens 162-201 16816114-0 2006 Reactive oxygen species mediates disialoganglioside GD3-induced inhibition of ERK1/2 and matrix metalloproteinase-9 expression in vascular smooth muscle cells. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 3 Homo sapiens 78-84 16511354-7 2006 The activation of tissue transglutaminase and ERK1/2 by MTX was sup-pressed by BAPTA-AM or ROS scavengers. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 3 Homo sapiens 46-52 16511354-9 2006 These results suggest that [Ca(2+)]-dependent generation of in-tracellular ROS, at least in part, play an important role in MTX-stimulated cellular responses, such as activation of tTGase, ERK phosphorylation, and in-duction of cell death, in human umbilical vein endothelial cells. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 3 Homo sapiens 189-192 16211253-8 2005 These findings suggest that sodium salicylate partially activates HSF1 via ROS production and p38MAPK activation and the salicylate-induced inert HSF1 can be fully activated into a transcriptionally competent form by the ERK1/2 signaling pathways that are activated independently of ROS during SR. Reactive Oxygen Species 283-286 mitogen-activated protein kinase 3 Homo sapiens 221-227 16081426-0 2005 Platelet-derived growth factor and reactive oxygen species (ROS) regulate Ras protein levels in primary human fibroblasts via ERK1/2. Reactive Oxygen Species 60-63 mitogen-activated protein kinase 3 Homo sapiens 126-132 15888667-7 2005 This study indicates that OCs strongly activate the ERK1/2 pathway, and it identifies a critical role of ROS in OC-induced ERK activation, probably by stabilizing its phosphorylation. Reactive Oxygen Species 105-108 mitogen-activated protein kinase 3 Homo sapiens 52-58 16109307-10 2005 ERK 1/2, PI 3 K, p38 MAPK, and MLCK inhibitors prevent these ROS generators from inducing the TEER decrease. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 3 Homo sapiens 0-7 16109307-10 2005 ERK 1/2, PI 3 K, p38 MAPK, and MLCK inhibitors prevent these ROS generators from inducing the TEER decrease. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 3 Homo sapiens 21-25 16049136-7 2005 We conclude that activation of tie-2 receptors by Ang-1 triggers the production of ROS through activation of NADPH oxidase and that ROS generation by Ang-1 promotes endothelial cell migration while negatively regulating Erk1/2 phosphorylation. Reactive Oxygen Species 132-135 mitogen-activated protein kinase 3 Homo sapiens 220-226 15870884-11 2005 The above results suggest that ROS induces uPAR expression via Erk-1/2 and AP-1 signaling pathways and, in turn, stimulates the cell invasiveness in human gastric cancer AGS cells. Reactive Oxygen Species 31-34 mitogen-activated protein kinase 3 Homo sapiens 63-70 15863496-1 2005 Carbon monoxide (CO), one of the end products of heme oxygenase activity, inhibits smooth muscle proliferation by decreasing ERK1/2 phosphorylation and cyclin D1 expression, a signaling pathway that is known to be modulated by reactive oxygen species (ROS) in airway smooth muscle cells (ASMCs). Reactive Oxygen Species 227-250 mitogen-activated protein kinase 3 Homo sapiens 125-131 15795063-0 2005 Benzoquinone activates the ERK/MAPK signaling pathway via ROS production in HL-60 cells. Reactive Oxygen Species 58-61 mitogen-activated protein kinase 3 Homo sapiens 31-35 15795063-3 2005 Therefore, we explored the mechanisms underlying BQ-induced HL-60 cell proliferation by studying the role of BQ-induced reactive oxygen species (ROS) in the activation of the ERK-MAPK signaling pathway. Reactive Oxygen Species 145-148 mitogen-activated protein kinase 3 Homo sapiens 179-183 15841469-10 2005 In conclusion, our findings suggest that MMP-2 is required for the mitogenic and proinvasive effects of ROS on HSC and demonstrate that ERK1/2 and PI3K are the main signals involved in ROS-mediated MMP-2 expression. Reactive Oxygen Species 185-188 mitogen-activated protein kinase 3 Homo sapiens 136-142 15027896-10 2004 These results demonstrate that Ang II stimulates ERK1/ERK2 by AA and Nox4-derived reactive oxygen species, suggesting that these molecules act as downstream signal transducers of Ang II in the signalling pathway linking the Ang II receptor AT1 to ERK1/ERK2 activation. Reactive Oxygen Species 82-105 mitogen-activated protein kinase 3 Homo sapiens 49-53 15485492-5 2004 These effects depended on the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK1/2) pathway, as the specific MEK inhibitor, PD98059, prevented HaRas-mediated increase in ROS and superoxide anions. Reactive Oxygen Species 207-210 mitogen-activated protein kinase 3 Homo sapiens 113-119 15485492-8 2004 ROS generation induced by carbachol required the activation of ERK1/2 and PI3K. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 63-69 15203192-0 2004 Reactive oxygen species mediate Endothelin-1-induced activation of ERK1/2, PKB, and Pyk2 signaling, as well as protein synthesis, in vascular smooth muscle cells. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 3 Homo sapiens 67-73 15203192-3 2004 However, a possible role for ROS generation in mediating the ET-1 response on extracellular signal-regulated kinases 1 and 2 (ERK1/2), protein kinase B (PKB), and protein tyrosine kinase 2 (Pyk2), key components of the growth-promoting and proliferative signaling pathways, has not been examined in detail. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 3 Homo sapiens 126-132 15203192-4 2004 Our aim was to investigate the involvement of ROS in ET-1-mediated activation of ERK1/2, PKB, and Pyk2 in A-10 VSMCs. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 3 Homo sapiens 81-87 15829704-8 2005 Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2. Reactive Oxygen Species 25-48 mitogen-activated protein kinase 3 Homo sapiens 78-82 15829704-8 2005 Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2. Reactive Oxygen Species 25-48 mitogen-activated protein kinase 3 Homo sapiens 280-284 15829704-8 2005 Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2. Reactive Oxygen Species 50-53 mitogen-activated protein kinase 3 Homo sapiens 78-82 15829704-8 2005 Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2. Reactive Oxygen Species 50-53 mitogen-activated protein kinase 3 Homo sapiens 280-284 15778391-0 2005 NADPH oxidase-derived reactive oxygen species-mediated activation of ERK1/2 is required for apoptosis of human neutrophils induced by Entamoeba histolytica. Reactive Oxygen Species 22-45 mitogen-activated protein kinase 3 Homo sapiens 69-75 15778391-8 2005 Although E. histolytica strongly induced activation of ERK1/2 and p38 MAPK in neutrophils, the activation of ERK1/2 was closely associated with ROS-mediated apoptosis. Reactive Oxygen Species 144-147 mitogen-activated protein kinase 3 Homo sapiens 109-115 15778391-11 2005 These results strongly suggest that NADPH oxidase-derived ROS-mediated activation of ERK1/2 is required for the Entamoeba-induced neutrophil apoptosis. Reactive Oxygen Species 58-61 mitogen-activated protein kinase 3 Homo sapiens 85-91 15618548-7 2005 Intracellular ROS generation in response to LY83583 (O2 generator) or exogenous H2O2 and Ang II-induced ERK1/2 activation were unaltered by cytochalasin. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 3 Homo sapiens 104-110 15485497-9 2004 Our results indicate that neuronal death induced by GSH depletion is due to ROS-dependent activation of the ERK-1/2 signalling pathway in glial cells. Reactive Oxygen Species 76-79 mitogen-activated protein kinase 3 Homo sapiens 108-115 15382121-12 2004 The generation of ROS is essential for PTPase inactivation, receptor tyrosine kinase activation, and enhanced signaling down the ERK1/2 and AKT pathways. Reactive Oxygen Species 18-21 mitogen-activated protein kinase 3 Homo sapiens 129-135 15027896-10 2004 These results demonstrate that Ang II stimulates ERK1/ERK2 by AA and Nox4-derived reactive oxygen species, suggesting that these molecules act as downstream signal transducers of Ang II in the signalling pathway linking the Ang II receptor AT1 to ERK1/ERK2 activation. Reactive Oxygen Species 82-105 mitogen-activated protein kinase 3 Homo sapiens 247-251 15153095-5 2004 A variety of potential targets of reactive oxygen species and reactive nitrogen species could contribute to ERK1/2 activation. Reactive Oxygen Species 34-57 mitogen-activated protein kinase 3 Homo sapiens 108-114 15093752-0 2004 The hierarchical relationship between MAPK signaling and ROS generation in human leukemia cells undergoing apoptosis in response to the proteasome inhibitor Bortezomib. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 3 Homo sapiens 38-42 15167449-1 2004 OBJECTIVE: The role of reactive oxygen species (ROS) in mitogen-activated protein kinase (MAPK) signaling by angiotensin (Ang) II and endothelin-1 (ET-1) in human vascular smooth muscle cells (VSMC) was investigated. Reactive Oxygen Species 23-46 mitogen-activated protein kinase 3 Homo sapiens 90-94 15167449-1 2004 OBJECTIVE: The role of reactive oxygen species (ROS) in mitogen-activated protein kinase (MAPK) signaling by angiotensin (Ang) II and endothelin-1 (ET-1) in human vascular smooth muscle cells (VSMC) was investigated. Reactive Oxygen Species 48-51 mitogen-activated protein kinase 3 Homo sapiens 90-94 12881478-8 2003 These data indicate that pathophysiological levels of Hcy can alter human monocyte function by upregulating MCP-1 and IL-8 expression and secretion via enhanced formation of intracellular ROS originated from NAD(P)H oxidase source via calmodulin or protein kinase C signaling pathways and that Hcy-induced ROS subsequently activates mitogen-activated protein kinase (p38 and ERK1/2) and nuclear factor-kappaB in a PPARgamma activator-sensitive manner. Reactive Oxygen Species 188-191 mitogen-activated protein kinase 3 Homo sapiens 375-381 14680682-6 2003 Proliferation-associated extracellular ROS generation is mediated through mitogenic signaling pathways, involving ERK1/2 and PKC, but is independent of de novo DNA synthesis, gene expression and protein synthesis. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 3 Homo sapiens 114-120 12840032-0 2003 Constitutive induction of p-Erk1/2 accompanied by reduced activities of protein phosphatases 1 and 2A and MKP3 due to reactive oxygen species during cellular senescence. Reactive Oxygen Species 118-141 mitogen-activated protein kinase 3 Homo sapiens 28-34 14623829-8 2003 In summary, we demonstrate for the first time that resveratrol inhibits strain-induced ET-1 gene expression, partially by interfering with the ERK1/2 pathway through attenuation of reactive oxygen species formation. Reactive Oxygen Species 181-204 mitogen-activated protein kinase 3 Homo sapiens 143-149 14516795-2 2003 Arsenite treatment resulted in the persistent activation of p70(s6k) and extracellular signal-regulated kinase 1/2 (ERK1/2) which was accompanied by an increase in intracellular ROS production. Reactive Oxygen Species 178-181 mitogen-activated protein kinase 3 Homo sapiens 116-122 12840032-9 2003 In summary, SA-p-Erk1/2 was most likely due to the oxidation of PP1/2A, which resulted from the continuous exposure of the cells to vast amounts of ROS generated during cellular senescence by oxidation of Cys62 and Cys105 in PP1C-alpha and metal ion(s). Reactive Oxygen Species 148-151 mitogen-activated protein kinase 3 Homo sapiens 17-23 12529294-5 2003 We subsequently investigated the signal transduction pathways involved in ROS generation and demonstrated that fMLP-stimulated ROS production was inhibited by the phosphatidylinositol 3 kinase (PI3K) inhibitor LY294002, but not by the MAPK/ERK kinase (MEK) inhibitor U0126. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 3 Homo sapiens 235-239 12594056-10 2003 Taken together, our data suggest that hyperoxia, by virtue of activating NADPH oxidase, generates reactive oxygen species (ROS), which mediates cell death of lung epithelium via ERK1/2 MAPK activation, and functions upstream of caspase activation in lung epithelial cells. Reactive Oxygen Species 98-121 mitogen-activated protein kinase 3 Homo sapiens 178-184 12594056-10 2003 Taken together, our data suggest that hyperoxia, by virtue of activating NADPH oxidase, generates reactive oxygen species (ROS), which mediates cell death of lung epithelium via ERK1/2 MAPK activation, and functions upstream of caspase activation in lung epithelial cells. Reactive Oxygen Species 98-121 mitogen-activated protein kinase 3 Homo sapiens 185-189 12594056-10 2003 Taken together, our data suggest that hyperoxia, by virtue of activating NADPH oxidase, generates reactive oxygen species (ROS), which mediates cell death of lung epithelium via ERK1/2 MAPK activation, and functions upstream of caspase activation in lung epithelial cells. Reactive Oxygen Species 123-126 mitogen-activated protein kinase 3 Homo sapiens 178-184 12594056-10 2003 Taken together, our data suggest that hyperoxia, by virtue of activating NADPH oxidase, generates reactive oxygen species (ROS), which mediates cell death of lung epithelium via ERK1/2 MAPK activation, and functions upstream of caspase activation in lung epithelial cells. Reactive Oxygen Species 123-126 mitogen-activated protein kinase 3 Homo sapiens 185-189 12878040-9 2003 Based on these findings we propose a mechanism involving tyrosine kinases, PI3 kinase, and the ERK1/2 pathway, leading to activation of the NADPH oxidase and production of ROS in neutrophils stimulated by organic solvents. Reactive Oxygen Species 172-175 mitogen-activated protein kinase 3 Homo sapiens 95-101 12732205-5 2003 Chronic exposure to high glucose resulted in enhancement of generation of reactive oxygen species (ROS), as determined by increasing level of 2,7-dichlorofluorescein (DCF), and subsequent activation of p38 mitogen-activated protein kinase (MAPK). Reactive Oxygen Species 99-102 mitogen-activated protein kinase 3 Homo sapiens 240-244 12681287-4 2003 NADPH oxidase activation and, therefore, the production of ROS were shown to be involved in the increase of alpha2beta1-integrin plasma membrane expression, p38 MAPK phosphorylation, cyclin expression, and G1/S transition. Reactive Oxygen Species 59-62 mitogen-activated protein kinase 3 Homo sapiens 161-165 11994490-4 2002 At these concentrations, cyPGs induce production of reactive oxygen species, thereby synergizing with TNF-alpha to activate the extracellular signal-regulated kinase 1/2, an activation which in turn potentiates proinflammatory cytokine expression at both transcriptional and posttranscriptional levels. Reactive Oxygen Species 52-75 mitogen-activated protein kinase 3 Homo sapiens 128-169 12482247-1 2002 Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1). Reactive Oxygen Species 166-169 mitogen-activated protein kinase 3 Homo sapiens 40-46 12482247-1 2002 Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1). Reactive Oxygen Species 166-169 mitogen-activated protein kinase 3 Homo sapiens 128-132 11406464-4 2001 Reactive oxygen species (ROS) were also demonstrated to be associated with TGS-induced ERK1/2 phosphorylation. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 3 Homo sapiens 87-93 11641267-8 2001 Our data indicate that p90RSK downstream of ERK1/2 is the molecular target for ROS generated through stimulation of purinergic receptors by ATP. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 3 Homo sapiens 44-50 11406464-4 2001 Reactive oxygen species (ROS) were also demonstrated to be associated with TGS-induced ERK1/2 phosphorylation. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 3 Homo sapiens 87-93 11406464-7 2001 Our study demonstrated the essential role of G proteins, NO, and ROS in TGS-dependent ERK1/2 activation and proliferative response in vascular endothelial cells. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 3 Homo sapiens 86-92 11369207-11 2001 Ki-Ras, on the other hand, stimulates the scavenging of ROS by activating posttranscriptionally the mitochondrial antioxidant enzyme, Mn-superoxide dismutase (Mn-SOD), via an ERK1/2-dependent pathway. Reactive Oxygen Species 56-59 mitogen-activated protein kinase 3 Homo sapiens 175-181 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. Reactive Oxygen Species 22-25 mitogen-activated protein kinase 3 Homo sapiens 168-174 11310789-9 2001 These findings suggest that a single UVA irradiation-induced melanogenesis is associated with the activation of ERK1/2 by upstream signals that originate from reactive oxygen species or from activated tyrosine kinase receptors, but not from damaged DNA. Reactive Oxygen Species 159-182 mitogen-activated protein kinase 3 Homo sapiens 112-118 10641711-3 1999 We have recently shown that exposure of human keratinocytes to physiologic doses of ultraviolet B radiation (UVB) activates epidermal growth factor receptor (EGFR)/extracellular-regulated kinase 1 and 2 (ERK1/2), and p38 signaling pathways via reactive oxygen species. Reactive Oxygen Species 244-267 mitogen-activated protein kinase 3 Homo sapiens 204-210 11182298-1 2001 We have recently shown that exposure of human keratinocytes to physiologic doses of ultraviolet B (UVB) activates epidermal growth factor receptor (EGFR)/extracellular-regulated kinases 1 and 2 (ERK1/2) and p38 signaling pathways via reactive oxygen species, an effect that can be modulated by antioxidants. Reactive Oxygen Species 234-257 mitogen-activated protein kinase 3 Homo sapiens 195-201 10669634-8 2000 However, simultaneous blockade of the ERK1/2 and ROS pathways by using PD098059 combined with diphenylene iodonium or N-acetylcysteine potently enhanced the ability of MAPK kinase inhibitors to abrogate MCP-1 mRNA expression (100+/-2% inhibition). Reactive Oxygen Species 49-52 mitogen-activated protein kinase 3 Homo sapiens 168-172 15693275-3 2000 Several intracellular signal events stimulated by ROS have been defined, including the identification of two members of the mitogen activated protein kinase family (ERK1/2 and big MAP kinase, BMK1), tyrosine kinases (Src and Syk) and different isoenzymes of PKC as redox-sensitive kinases. Reactive Oxygen Species 50-53 mitogen-activated protein kinase 3 Homo sapiens 165-171 9489720-6 1998 Hippocampal slices exposed to various ROS and NO donors resulted in increases in levels of the active forms of both p42 MAPK and p44 MAPK. Reactive Oxygen Species 38-41 mitogen-activated protein kinase 3 Homo sapiens 129-137 10233767-0 1999 UVB activates ERK1/2 and p38 signaling pathways via reactive oxygen species in cultured keratinocytes. Reactive Oxygen Species 52-75 mitogen-activated protein kinase 3 Homo sapiens 14-20 10233767-10 1999 These findings demonstrate that reactive oxygen species are important multifunctional mediators of ultraviolet B-induced ERK1/2 and p38 signaling transduction pathways and suggest that ERK1/2 may play an important part in protecting keratinocytes from cell death following oxidative stress. Reactive Oxygen Species 32-55 mitogen-activated protein kinase 3 Homo sapiens 121-127 9489720-7 1998 The ROS- and NO-enhanced tyrosine phosphorylation and activation of p42 MAPK and p44 MAPK were inhibited by pretreatment with the antioxidant N-acetyl-L-cysteine. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 3 Homo sapiens 81-89 9489720-8 1998 Our observations indicate that ROS and NO can mediate protein tyrosine phosphorylation and MAPK signaling in the hippocampus via a redox-sensitive mechanism and suggest a potential cellular mechanism for their effects in the nervous system. Reactive Oxygen Species 31-34 mitogen-activated protein kinase 3 Homo sapiens 91-95 34768994-4 2021 HP-NAP-induced ROS production in ATRA-induced differentiated HL-60 cells is mediated by the PTX-sensitive heterotrimeric G protein-dependent activation of extracellular signal-regulated kinase 1/2 and p38-mitogen-activated protein kinase, which is consistent with the findings reported for human neutrophils. Reactive Oxygen Species 15-18 mitogen-activated protein kinase 3 Homo sapiens 155-196 34634453-12 2021 Further, NETs promoted trophoblast apoptosis by activating the ROS-dependent mitochondrial pathway, which is mediated by ERK1/2 signalling. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 3 Homo sapiens 121-127 34749347-0 2021 DOX-loaded silver nanotriangles and photothermal therapy exert a synergistic antibreast cancer effect via ROS/ERK1/2 signaling pathway. Reactive Oxygen Species 106-109 mitogen-activated protein kinase 3 Homo sapiens 110-116 34749347-13 2021 The synergy might be closely associated with the excessive production of ROS, changed MMP and the activation of ERK1/2 signaling pathway. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 3 Homo sapiens 112-118 34487308-10 2021 The evaluation of Erk1/2 in the presence and absence of Na-Pyruvate, PEG-Catalase, and PD98059 established ROS-Erk1/2 participation in autophagy regulation. Reactive Oxygen Species 107-110 mitogen-activated protein kinase 3 Homo sapiens 111-117 34248106-8 2021 In contrast, cis-palmitoleic acid inactivated MAPK/ERK1/2, leading to increased ROS generation. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 3 Homo sapiens 46-50 34248106-8 2021 In contrast, cis-palmitoleic acid inactivated MAPK/ERK1/2, leading to increased ROS generation. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 3 Homo sapiens 51-57 35294968-8 2022 Further, our findings revealed ROS-p38-Erk1/2 involvement. Reactive Oxygen Species 31-34 mitogen-activated protein kinase 3 Homo sapiens 39-45 34439417-7 2021 The cellular components mediating the downregulation of ROS included extracellular signal-regulated kinase 1/2 (ERK1/2), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and uncoupling protein 2 (UCP2). Reactive Oxygen Species 56-59 mitogen-activated protein kinase 3 Homo sapiens 112-118 35563563-8 2022 ROS/MAPK (p38 MAPK, Erk1/2) and ROS functioned as upstream signaling of AP-1 and NF-kappaB, respectively. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 20-26 35563563-9 2022 Sulforaphane suppresses the nicotine-induced MMP-9 by inhibiting ROS-mediated MAPK (p38 MAPK, Erk1/2)/AP-1 and ROS-mediated NF-kappaB signaling axes, which in turn inhibit cell invasion in human gastric cancer AGS cells. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 3 Homo sapiens 94-100 33819767-9 2021 In MCF-7 cells, G-Rg2 increased ROS production by inhibiting ERK1/2 and Akt activation. Reactive Oxygen Species 32-35 mitogen-activated protein kinase 3 Homo sapiens 61-67 35453328-0 2022 Ginsenoside Rh1 Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cell Migration and Proliferation through Suppression of the ROS-Mediated ERK1/2/p90RSK/KLF4 Signaling Pathway. Reactive Oxygen Species 131-134 mitogen-activated protein kinase 3 Homo sapiens 144-150 35453328-13 2022 In conclusion, Rh1 inhibited the Ang II-induced migration and proliferation of RASMCs by suppressing the ROS-mediated ERK1/2/p90RSK signaling pathway. Reactive Oxygen Species 105-108 mitogen-activated protein kinase 3 Homo sapiens 118-124 35464760-0 2022 Thyroid Cancer-Associated Mitochondrial DNA Mutation G3842A Promotes Tumorigenicity via ROS-Mediated ERK1/2 Activation. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 3 Homo sapiens 101-107 35464760-8 2022 By contrast, the levels of reactive oxygen species (ROS) were increased to activate extracellular signal-regulated kinase (ERK1/2) signaling, which contributed to tumorigenicity. Reactive Oxygen Species 27-50 mitogen-activated protein kinase 3 Homo sapiens 123-129 35464760-8 2022 By contrast, the levels of reactive oxygen species (ROS) were increased to activate extracellular signal-regulated kinase (ERK1/2) signaling, which contributed to tumorigenicity. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 3 Homo sapiens 123-129 31254584-8 2019 Furthermore, we also detected a potent activation of the ERK1/2 kinase, which suggested the induction of reactive oxygen species (ROS). Reactive Oxygen Species 105-128 mitogen-activated protein kinase 3 Homo sapiens 57-63 33553145-6 2020 This inhibition of ROS initiated by MEK1/2-ERK1/2 may serve as a negative feedback loop from the MAPK pathway toward FGFR1 and PI3K/AKT activation. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 3 Homo sapiens 43-49 33471797-8 2021 Taken together, these results indicate that ROS activation and ROS-mediated phosphorylated ERK1/2 activation are essential to activate autophagy, resulting in the apoptosis of PFOS-treated RTCs. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 3 Homo sapiens 91-97 32251677-2 2020 Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known to enhance many neutrophil functions such as reactive oxygen species (ROS) production, degranulation and cell survival via the activation of the ERK1/2 pathway. Reactive Oxygen Species 112-135 mitogen-activated protein kinase 3 Homo sapiens 212-218 32251677-2 2020 Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known to enhance many neutrophil functions such as reactive oxygen species (ROS) production, degranulation and cell survival via the activation of the ERK1/2 pathway. Reactive Oxygen Species 137-140 mitogen-activated protein kinase 3 Homo sapiens 212-218 32251677-3 2020 ERK1/2 pathway activation is redox sensitive and could be modulated by ROS. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 3 Homo sapiens 0-6 32251677-4 2020 In order to investigate whether NADPH oxidase NOX2-derived ROS could contribute to GM-CSF-induced ERK1/2 phosphorylation, we tested the effect of two selective NOX2 inhibitors, diphenylene iodonium (DPI) and apocynin. Reactive Oxygen Species 59-62 mitogen-activated protein kinase 3 Homo sapiens 98-104 32431605-5 2020 We found that DHA induced ROS production, caused mitochondrial damage, and activated autophagy via stimulation of the ROS/Erk1/2 pathway. Reactive Oxygen Species 118-121 mitogen-activated protein kinase 3 Homo sapiens 122-128 30464227-5 2019 Moreover, inhibition of phosphorylated ERK1/2 (pERK1/2) resulted in decreased ROS and Nox4 levels, indicating the mutual dependency between pERK1/2 and Nox4-derived ROS during neurogenesis. Reactive Oxygen Species 165-168 mitogen-activated protein kinase 3 Homo sapiens 39-45 33828192-9 2021 In summary, our findings show that exposure to 1760 MHz RF-EMF induces ROS generation, leading to MMP activation and FoxO3a and ERK1/2 phosphorylation. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 3 Homo sapiens 128-134 33522955-13 2021 Our study demonstrated that the overexpression of FOXC1 that was induced by the ROS dependent on the extracellular regulated protein kinases 1 and 2 (ERK1/2)- phospho-ETS Transcription Factor 1 (p-ELK1) pathway. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 3 Homo sapiens 101-148 33522955-13 2021 Our study demonstrated that the overexpression of FOXC1 that was induced by the ROS dependent on the extracellular regulated protein kinases 1 and 2 (ERK1/2)- phospho-ETS Transcription Factor 1 (p-ELK1) pathway. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 3 Homo sapiens 150-156 33109619-9 2021 These studies provide mechanistic information on a novel chemical scaffold that selectively regulates ERK1/2-targeted transcription factors and inhibits the proliferation of A375 melanoma cells through a ROS-dependent mechanism. Reactive Oxygen Species 204-207 mitogen-activated protein kinase 3 Homo sapiens 102-108 32813234-0 2020 Quercetin Ameliorates CFA-Induced Chronic Inflammatory Hyperalgesia via Modulation of ROS-Mediated ERK1/2 Signaling and Inhibition of Spinal Glial Activation In Vivo. Reactive Oxygen Species 86-89 mitogen-activated protein kinase 3 Homo sapiens 99-105 32813234-6 2020 The insight of molecular signaling during chronic hyperalgesia was analyzed by TNF-alpha-TNFR1-ERK1/2 pathway in relation to change in ROS level in DRG and spinal cord. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 3 Homo sapiens 95-101 32521698-9 2020 Chrysosplenol d activated ERK1/2, but not other kinases tested, increased cytosolic reactive oxygen species (ROS) and induced autophagy in MDA-MB-231 cells. Reactive Oxygen Species 84-107 mitogen-activated protein kinase 3 Homo sapiens 26-32 32521698-9 2020 Chrysosplenol d activated ERK1/2, but not other kinases tested, increased cytosolic reactive oxygen species (ROS) and induced autophagy in MDA-MB-231 cells. Reactive Oxygen Species 109-112 mitogen-activated protein kinase 3 Homo sapiens 26-32 32119711-12 2020 Our data demonstrated that Ang II promotes ROS production and podocytes injury through activation of Arf6-Erk1/2-Nox4 signaling. Reactive Oxygen Species 43-46 mitogen-activated protein kinase 3 Homo sapiens 106-112 32411325-0 2020 Neochamaejasmin A Induces Mitochondrial-Mediated Apoptosis in Human Hepatoma Cells via ROS-Dependent Activation of the ERK1/2/JNK Signaling Pathway. Reactive Oxygen Species 87-90 mitogen-activated protein kinase 3 Homo sapiens 119-125 32411325-11 2020 These results implied that NCA induced mitochondrial-mediated cell apoptosis via ROS-dependent activation of the ERK1/2/JNK signaling pathway in HepG2 cells. Reactive Oxygen Species 81-84 mitogen-activated protein kinase 3 Homo sapiens 113-119 31129114-0 2019 ML171, a specific inhibitor of NOX1 attenuates formalin induced nociceptive sensitization by inhibition of ROS mediated ERK1/2 signaling. Reactive Oxygen Species 107-110 mitogen-activated protein kinase 3 Homo sapiens 120-126 31129114-12 2019 The study for the first time depicts anti-nociceptive potential of ML171 via regulation of ROS mediated ERK1/2 signaling by inhibition of NOX1 activity. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 3 Homo sapiens 104-110 31238089-5 2019 Activation of MAPKs (ERK1/2, JNK, and p38) by ROS is essential and contribute to osteoclast differentiation. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 3 Homo sapiens 21-27 30464227-4 2019 Importantly, a novel interaction between Vps26a and Nox4 linked to the activation of ERK1/2 depended highly on ROS levels during neurogenesis, which were strongly suppressed in differentiating Vps26a-/- ESCs. Reactive Oxygen Species 111-114 mitogen-activated protein kinase 3 Homo sapiens 85-91 30464227-5 2019 Moreover, inhibition of phosphorylated ERK1/2 (pERK1/2) resulted in decreased ROS and Nox4 levels, indicating the mutual dependency between pERK1/2 and Nox4-derived ROS during neurogenesis. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 3 Homo sapiens 39-45 31026097-0 2019 alpha-Mangostin promotes apoptosis of human rheumatoid arthritis fibroblast-like synoviocytes by reactive oxygen species-dependent activation of ERK1/2 mitogen-activated protein kinase. Reactive Oxygen Species 97-120 mitogen-activated protein kinase 3 Homo sapiens 145-151 31254584-8 2019 Furthermore, we also detected a potent activation of the ERK1/2 kinase, which suggested the induction of reactive oxygen species (ROS). Reactive Oxygen Species 130-133 mitogen-activated protein kinase 3 Homo sapiens 57-63 30661992-5 2019 Using specific pharmacological inhibitors, we show that excess ROS production in both reticulocytes and mature SSRBCs is regulated by NADPH oxidases (NOXs), the mitogen-activated protein kinase (ERK1/2), and G-protein coupled-receptor kinase 2 (GRK2). Reactive Oxygen Species 63-66 mitogen-activated protein kinase 3 Homo sapiens 195-201 30628067-9 2019 ERK1/2 and Akt activation mediated the effect of ROS on NF-kappaB and HIF-1alpha and their pharmacological inhibition suppressed GEM-induced PTX3. Reactive Oxygen Species 49-52 mitogen-activated protein kinase 3 Homo sapiens 0-6 30661992-7 2019 Importantly, reducing ROS levels in SSRBCs with redox-active manganese (Mn) porphyrins, commonly known as mimics of superoxide dismutase (SOD), disrupted the cycle created by ROS by affecting NOX and GRK2 activities and ERK1/2 phosphorylation, thus abrogating RBC-endothelial interactions. Reactive Oxygen Species 175-178 mitogen-activated protein kinase 3 Homo sapiens 220-226 30661992-7 2019 Importantly, reducing ROS levels in SSRBCs with redox-active manganese (Mn) porphyrins, commonly known as mimics of superoxide dismutase (SOD), disrupted the cycle created by ROS by affecting NOX and GRK2 activities and ERK1/2 phosphorylation, thus abrogating RBC-endothelial interactions. Reactive Oxygen Species 22-25 mitogen-activated protein kinase 3 Homo sapiens 220-226 31261663-8 2019 The Nox-derived ROS signals promoted the activities of extracellular signal-regulated kinase 1/2 (ERK1/2). Reactive Oxygen Species 16-19 mitogen-activated protein kinase 3 Homo sapiens 98-104 31123601-9 2019 ROS production was also attenuated in the presence of an iron chelator, and after inhibition of either granzyme B or the ERK1/2 MAP kinase signaling pathway. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 121-127 30844388-8 2019 Furthermore, we found that angiotensin-(1-7) suppressed the abnormal calcium- and ROS-dependent activation of calcium/calmodulin-dependent protein kinase II delta (CaMKIIdelta), the increased expression of CaMKIIdelta-related proteins (NADPH oxidase 4 (Nox4), cellular communication network factor 2 (CTGF), and p-ERK1/2), and excessive collagen deposition in vitro and in vivo. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 3 Homo sapiens 314-320 30006481-3 2018 Apoptosis signal-regulating kinase 1 (ASK1) is a ubiquitously expressed mitogen-activated protein kinase (MAPK) kinase kinase (MAP3K) activated by various stress stimuli, including reactive oxygen species (ROS), tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS) and is known to regulate cell proliferation. Reactive Oxygen Species 181-204 mitogen-activated protein kinase 3 Homo sapiens 106-110 31024318-5 2019 Mechanistically, we found that knockdown of CCS decreases the activity of ERK1/2 mediated by the accumulation of ROS, which leads to the inhibition of cell proliferation and migration. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 3 Homo sapiens 74-80 31024318-6 2019 In summary, these results indicated that CCS promotes the growth and migration of breast cancer cells via regulating the ERK1/2 activity mediated by ROS. Reactive Oxygen Species 149-152 mitogen-activated protein kinase 3 Homo sapiens 121-127 30466984-0 2018 Naringenin suppresses growth of human placental choriocarcinoma via reactive oxygen species-mediated P38 and JNK MAPK pathways. Reactive Oxygen Species 68-91 mitogen-activated protein kinase 3 Homo sapiens 113-117 30236600-7 2018 The CS components activated the ROS-p38 MAPK-EMT pathway by increasing the level of phosphorylated p38 MAPK and p44/42 (ERK1/2), and by up-regulating Snail and Slug, the transcription factors for EMT. Reactive Oxygen Species 32-35 mitogen-activated protein kinase 3 Homo sapiens 40-44 30236600-7 2018 The CS components activated the ROS-p38 MAPK-EMT pathway by increasing the level of phosphorylated p38 MAPK and p44/42 (ERK1/2), and by up-regulating Snail and Slug, the transcription factors for EMT. Reactive Oxygen Species 32-35 mitogen-activated protein kinase 3 Homo sapiens 120-126 30037475-8 2018 It was concluded that exposure of chondrocytes to LIPUS led to reactive oxygen species generation, which activated MAPK signaling and further increased chondrocyte-specific gene markers involved in chondrocyte differentiation and extracellular matrix formation. Reactive Oxygen Species 63-86 mitogen-activated protein kinase 3 Homo sapiens 115-119 30735839-7 2019 Furthermore, we demonstrate that SNG induces ROS-depended extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylation, and prostate apoptosis response-4 (Par-4) cleavage, leading to the induction of apoptosis in human prostate cancer cells. Reactive Oxygen Species 45-48 mitogen-activated protein kinase 3 Homo sapiens 100-106 30776374-6 2019 GCN5L1 knockdown in cardiac-derived AC16 cells was associated with reduced activation of the pro-survival MAP kinase ERK1/2, which was also reversed by ROS scavenging, leading to restored cell viability. Reactive Oxygen Species 152-155 mitogen-activated protein kinase 3 Homo sapiens 117-123 30701573-13 2019 Anti-beta2 GPI/beta2 GPI induced ROS generation without relying on NADPH oxidase, which contributes to NETosis independently of ERK1/2, Zn2+ , or AKT. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 3 Homo sapiens 128-134 30811039-4 2019 Reactive oxygen species (ROS) are a common subproduct of oxidative energy metabolism and are considered to be a significant physiological modulator of several intracellular signaling pathways including the MAPK pathway. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 3 Homo sapiens 206-210 30811039-4 2019 Reactive oxygen species (ROS) are a common subproduct of oxidative energy metabolism and are considered to be a significant physiological modulator of several intracellular signaling pathways including the MAPK pathway. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 3 Homo sapiens 206-210 30359932-9 2019 In conclusion, the complex exhibits more potent cytotoxicity than piplartine in a panel of different cancer cells and triggers ROS/ERK/p38-mediated apoptosis in HL-60 cells. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 3 Homo sapiens 131-134 29906487-4 2018 Mechanistically, DFO significantly activated ERK1/2 signaling, which is reactive oxygen species (ROS)-dependent. Reactive Oxygen Species 72-95 mitogen-activated protein kinase 3 Homo sapiens 45-51 29906487-4 2018 Mechanistically, DFO significantly activated ERK1/2 signaling, which is reactive oxygen species (ROS)-dependent. Reactive Oxygen Species 97-100 mitogen-activated protein kinase 3 Homo sapiens 45-51 30006481-3 2018 Apoptosis signal-regulating kinase 1 (ASK1) is a ubiquitously expressed mitogen-activated protein kinase (MAPK) kinase kinase (MAP3K) activated by various stress stimuli, including reactive oxygen species (ROS), tumor necrosis factor (TNF)-alpha, and lipopolysaccharide (LPS) and is known to regulate cell proliferation. Reactive Oxygen Species 206-209 mitogen-activated protein kinase 3 Homo sapiens 106-110 29549478-0 2018 Metformin Promotes HaCaT Cell Apoptosis through Generation of Reactive Oxygen Species via Raf-1-ERK1/2-Nrf2 Inactivation. Reactive Oxygen Species 62-85 mitogen-activated protein kinase 3 Homo sapiens 96-102 29627441-10 2018 Therefore, we studied the effect of ROS-related signaling on Nrf2 by measuring the activation of AKT and members of the mitogen-activated protein kinase family, such as extracellular signal-regulated kinase (ERK1/2) and p38. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 3 Homo sapiens 208-214 30011321-9 2018 Notably, intracellular reactive oxygen species levels decreased and phosphorylation of Akt and Erk1/2 increased in cells exposed to an EMF, suggesting that reduced levels of intracellular reactive oxygen species play a role in increased proliferation. Reactive Oxygen Species 188-211 mitogen-activated protein kinase 3 Homo sapiens 95-101 29672044-11 2018 NOX-derived ROS and Src/MAPKs (Erk1/2 and p38 MAPK) functioned as upstream activators of NF-kappaB and AP-1, respectively. Reactive Oxygen Species 12-15 mitogen-activated protein kinase 3 Homo sapiens 31-37 29084209-4 2018 ROS, such as H2O2, are important for carcinogenesis and activate MAPK signaling pathways. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 65-69 29140787-8 2018 Finally, the inhibition of these canonical and non-canonical pathways did not decrease the ROS increment, while the inhibition of ROS production entirely abolished the phosphorylation of Smad3, ERK1/2 and JNK1/2. Reactive Oxygen Species 130-133 mitogen-activated protein kinase 3 Homo sapiens 194-200 29768263-0 2018 Fibrinopeptide A Induces Expression of C-Reactive Protein via the ROS-ERK1/2/ P38-NF-kappaB Signal Pathway in Vascular Smooth Muscle Cells. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 3 Homo sapiens 70-76 29568362-6 2018 The antitumor activity was partly due to NO-cGMP dependent pathway, contributing to reduced cell number and apoptosis, and partly to the salicylaldehyde moiety and reactive oxygen species (ROS) activated ERK1/2 signaling converging on p53 dependent caspase-3 cleavage. Reactive Oxygen Species 164-187 mitogen-activated protein kinase 3 Homo sapiens 204-210 29568362-6 2018 The antitumor activity was partly due to NO-cGMP dependent pathway, contributing to reduced cell number and apoptosis, and partly to the salicylaldehyde moiety and reactive oxygen species (ROS) activated ERK1/2 signaling converging on p53 dependent caspase-3 cleavage. Reactive Oxygen Species 189-192 mitogen-activated protein kinase 3 Homo sapiens 204-210 29768263-15 2018 CONCLUSIONS: FPA induces CRP expression in VSMCs via ROS-ERK1/2/p38-NF-kappaB signal pathway. Reactive Oxygen Species 53-56 mitogen-activated protein kinase 3 Homo sapiens 57-63 29136006-8 2017 The effects of LPS were associated with phosphorylation of Akt, ERK1/2 and PLA2 in stimulated platelets, and inhibitors of PI3-kinase, Akt and ERK1/2 reduced significantly LPS enhanced platelet function and associated ROS production. Reactive Oxygen Species 218-221 mitogen-activated protein kinase 3 Homo sapiens 143-149 28876465-5 2018 Additional molecular studies revealed that B2G2-induced cell death was mediated mainly through ROS-induced sustained activation of ERK1/2, which was due to inhibition of MAP kinase phosphatase (MKP) activity as over-expression of MKP3 in LNCaP cells conferred significant protection against B2G2-induced cell death. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 3 Homo sapiens 131-137 29423117-8 2018 Our study suggests that excessive intracellular ROS can trigger the exit from stem cell state and promote the neuronal differentiation of hESCs, and that MAPK-ERK1/2 signaling may play a proactive role in the ROS-induced neuronal differentiation of hESCs. Reactive Oxygen Species 209-212 mitogen-activated protein kinase 3 Homo sapiens 159-165 29375548-9 2017 Finally, we demonstrate that increased mitochondrial ROS enhanced phosphorylation of ERK1/2, and induced production of IL8, findings that correlate with previous observations of increased MAPK activation and inflammatory cytokine production in CGD cells. Reactive Oxygen Species 53-56 mitogen-activated protein kinase 3 Homo sapiens 85-91 29375548-9 2017 Finally, we demonstrate that increased mitochondrial ROS enhanced phosphorylation of ERK1/2, and induced production of IL8, findings that correlate with previous observations of increased MAPK activation and inflammatory cytokine production in CGD cells. Reactive Oxygen Species 53-56 mitogen-activated protein kinase 3 Homo sapiens 188-192 29022012-8 2017 Likewise, MAPK inhibitors effectively suppressed vanadium-induced apoptosis and ROS generation (P < 0.05). Reactive Oxygen Species 80-83 mitogen-activated protein kinase 3 Homo sapiens 10-14 29136006-10 2017 We therefore conclude that LPS increases human platelet activation through a TLR4-PI3K-Akt-ERK1/2-PLA2 -dependent pathway that is dependent on ROS and TXA2 formation. Reactive Oxygen Species 143-146 mitogen-activated protein kinase 3 Homo sapiens 91-97 29109418-1 2017 Recently, we identified a specific extremely low-frequency pulsed electromagnetic field (ELF-PEMF) that supports human osteoblast (hOBs) function in an ERK1/2-dependent manner, suggesting reactive oxygen species (ROS) being key regulators in this process. Reactive Oxygen Species 188-211 mitogen-activated protein kinase 3 Homo sapiens 152-158 29109418-1 2017 Recently, we identified a specific extremely low-frequency pulsed electromagnetic field (ELF-PEMF) that supports human osteoblast (hOBs) function in an ERK1/2-dependent manner, suggesting reactive oxygen species (ROS) being key regulators in this process. Reactive Oxygen Species 213-216 mitogen-activated protein kinase 3 Homo sapiens 152-158 28969111-10 2017 CONCLUSION: Citral protects against high glucose induced oxidative stress through inhibiting ROS activated MAPK signaling pathway in HepG2 cells. Reactive Oxygen Species 93-96 mitogen-activated protein kinase 3 Homo sapiens 107-111 28545088-11 2017 Together our data demonstrate that resistance to PDT is in part mediated by the activation of a ROS-ERK1/2-HIF-1 axis, thus, identifying novel therapeutic targets that could be used in combination with PDT. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 3 Homo sapiens 100-106 28476123-10 2017 The upregulation of reactive oxygen species (ROS) induced sustained ERK1/2 activation participated in G-1 induced cell growth arrest. Reactive Oxygen Species 20-43 mitogen-activated protein kinase 3 Homo sapiens 68-74 28476123-10 2017 The upregulation of reactive oxygen species (ROS) induced sustained ERK1/2 activation participated in G-1 induced cell growth arrest. Reactive Oxygen Species 45-48 mitogen-activated protein kinase 3 Homo sapiens 68-74 28427390-12 2017 AGEs also increased phosphorylation of the mitogen-activated protein kinases p38 and ERK1/2, whereas the specific inhibitors of p38, ERK1/2, and TTFA effectively blocked AGEs-induced reactive oxygen species production and eNOS downregulation. Reactive Oxygen Species 183-206 mitogen-activated protein kinase 3 Homo sapiens 133-139 27838900-8 2017 On the other hand, IFN-gamma resulted in ROS generation, through H2O2 production, whereas pre-treatment with the ROS inhibitor NAC caused ROS inhibition and a significant decrease in the phosphorylation levels of AKT, ERK1/2, p38 and STAT1. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 3 Homo sapiens 218-224 28423696-6 2017 Chelating intracellular calcium with Bapta-AM or inhibiting ERK1/2 with PD98059 significantly potentiated dexamethasone-induced mitochondrial membrane potential collapse, reactive oxygen species production, cytochrome c release, caspase-3 activity, and cell death. Reactive Oxygen Species 171-194 mitogen-activated protein kinase 3 Homo sapiens 60-66 26892626-8 2017 We observed that PINK1 stabilization was selectively regulated by ROS-mediated c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling activation but not p38 signaling. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 3 Homo sapiens 156-162 28443465-8 2017 Moreover, bauerenol treatment activates p38MAPK and inactivates the anti-apoptotic kinases Akt and ERK1/2 through the induction of reactive oxygen species. Reactive Oxygen Species 131-154 mitogen-activated protein kinase 3 Homo sapiens 99-105 27838900-8 2017 On the other hand, IFN-gamma resulted in ROS generation, through H2O2 production, whereas pre-treatment with the ROS inhibitor NAC caused ROS inhibition and a significant decrease in the phosphorylation levels of AKT, ERK1/2, p38 and STAT1. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 3 Homo sapiens 218-224 27271317-0 2017 Vasoactive intestinal peptide dampens formyl-peptide-induced ROS production and inflammation by targeting a MAPK-p47phox phosphorylation pathway in monocytes. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 3 Homo sapiens 108-112 27980400-0 2016 Cigarette smoke extract induces placental growth factor release from human bronchial epithelial cells via ROS/MAPK (ERK-1/2)/Egr-1 axis. Reactive Oxygen Species 106-109 mitogen-activated protein kinase 3 Homo sapiens 116-123 28111550-3 2016 ROS generation, by either H/R or the ROS donor xanthine oxidase-hypoxanthine (XO/HX) activated all three MAPKs (ERK1/2, JNK, p38), and induced Egr-1 expression and Egr-1 DNA-binding activity in CMECs, whereas ROS scavengers (EDA and NAC) had the opposite effect following H/R. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 112-118 28111550-3 2016 ROS generation, by either H/R or the ROS donor xanthine oxidase-hypoxanthine (XO/HX) activated all three MAPKs (ERK1/2, JNK, p38), and induced Egr-1 expression and Egr-1 DNA-binding activity in CMECs, whereas ROS scavengers (EDA and NAC) had the opposite effect following H/R. Reactive Oxygen Species 37-40 mitogen-activated protein kinase 3 Homo sapiens 112-118 28111550-3 2016 ROS generation, by either H/R or the ROS donor xanthine oxidase-hypoxanthine (XO/HX) activated all three MAPKs (ERK1/2, JNK, p38), and induced Egr-1 expression and Egr-1 DNA-binding activity in CMECs, whereas ROS scavengers (EDA and NAC) had the opposite effect following H/R. Reactive Oxygen Species 37-40 mitogen-activated protein kinase 3 Homo sapiens 112-118 26824338-6 2017 In LS174 cells, Lebein triggers the activation of the MAPK ERK1/2 pathway through induction of reactive oxygen species (ROS). Reactive Oxygen Species 95-118 mitogen-activated protein kinase 3 Homo sapiens 54-58 26824338-6 2017 In LS174 cells, Lebein triggers the activation of the MAPK ERK1/2 pathway through induction of reactive oxygen species (ROS). Reactive Oxygen Species 95-118 mitogen-activated protein kinase 3 Homo sapiens 59-65 26824338-6 2017 In LS174 cells, Lebein triggers the activation of the MAPK ERK1/2 pathway through induction of reactive oxygen species (ROS). Reactive Oxygen Species 120-123 mitogen-activated protein kinase 3 Homo sapiens 54-58 26824338-6 2017 In LS174 cells, Lebein triggers the activation of the MAPK ERK1/2 pathway through induction of reactive oxygen species (ROS). Reactive Oxygen Species 120-123 mitogen-activated protein kinase 3 Homo sapiens 59-65 26742524-7 2017 NADPH oxidase (Nox)- and mitochondrion-dependent ROS generation led to activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun-N-terminal kinase (JNK) and then activated the downstream transcriptional factors nuclear factor-kappaB (NF-kappaB) and c-Fos/activator protein 1 (AP-1), respectively. Reactive Oxygen Species 49-52 mitogen-activated protein kinase 3 Homo sapiens 128-134 26742524-9 2017 These results indicated that in brain astrocytes, activation of MAPK-mediated NF-kappaB and c-Fos/AP-1 cascades by Nox/ROS and mitoROS-dependent events is essential for HO-1 up-regulation induced by HG. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 3 Homo sapiens 64-68 27194217-9 2016 The role of extracellular signal-regulated kinase (ERK) 1/2 and/or ERK 5 signalling in PCB-induced ROS production was implicated through the reduction in ROS in the presence of the specific inhibitor U0126, whereas reduced ROS production after the use of SB203580 and SP600125 indicated the involvement of the p38 mitogen-activated protein kinase (MAPK) and c-Jun amino-terminal kinase (JNK) pathways, respectively. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 3 Homo sapiens 12-59 27194217-9 2016 The role of extracellular signal-regulated kinase (ERK) 1/2 and/or ERK 5 signalling in PCB-induced ROS production was implicated through the reduction in ROS in the presence of the specific inhibitor U0126, whereas reduced ROS production after the use of SB203580 and SP600125 indicated the involvement of the p38 mitogen-activated protein kinase (MAPK) and c-Jun amino-terminal kinase (JNK) pathways, respectively. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 3 Homo sapiens 348-352 27194217-9 2016 The role of extracellular signal-regulated kinase (ERK) 1/2 and/or ERK 5 signalling in PCB-induced ROS production was implicated through the reduction in ROS in the presence of the specific inhibitor U0126, whereas reduced ROS production after the use of SB203580 and SP600125 indicated the involvement of the p38 mitogen-activated protein kinase (MAPK) and c-Jun amino-terminal kinase (JNK) pathways, respectively. Reactive Oxygen Species 154-157 mitogen-activated protein kinase 3 Homo sapiens 12-59 27194217-9 2016 The role of extracellular signal-regulated kinase (ERK) 1/2 and/or ERK 5 signalling in PCB-induced ROS production was implicated through the reduction in ROS in the presence of the specific inhibitor U0126, whereas reduced ROS production after the use of SB203580 and SP600125 indicated the involvement of the p38 mitogen-activated protein kinase (MAPK) and c-Jun amino-terminal kinase (JNK) pathways, respectively. Reactive Oxygen Species 154-157 mitogen-activated protein kinase 3 Homo sapiens 12-59 27624867-12 2017 Taken together, our results reveal that alternol suppresses cell proliferation, migration and induces apoptosis, cell cycle arrest by modulating of ROS-dependent MAPK and STAT3 signalling pathways in human OS cells. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 3 Homo sapiens 162-166 27980400-4 2016 Herein, we investigated the effects of reactive oxygen species (ROS)-dependent activation of the mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase1/2 [ERK-1/2])/early growth response-1 (Egr-1) pathway on CSE-induced PlGF upregulation in human bronchial epithelium (HBE). Reactive Oxygen Species 39-62 mitogen-activated protein kinase 3 Homo sapiens 138-178 27980400-4 2016 Herein, we investigated the effects of reactive oxygen species (ROS)-dependent activation of the mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase1/2 [ERK-1/2])/early growth response-1 (Egr-1) pathway on CSE-induced PlGF upregulation in human bronchial epithelium (HBE). Reactive Oxygen Species 39-62 mitogen-activated protein kinase 3 Homo sapiens 180-187 27980400-4 2016 Herein, we investigated the effects of reactive oxygen species (ROS)-dependent activation of the mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase1/2 [ERK-1/2])/early growth response-1 (Egr-1) pathway on CSE-induced PlGF upregulation in human bronchial epithelium (HBE). Reactive Oxygen Species 64-67 mitogen-activated protein kinase 3 Homo sapiens 138-178 27980400-4 2016 Herein, we investigated the effects of reactive oxygen species (ROS)-dependent activation of the mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase1/2 [ERK-1/2])/early growth response-1 (Egr-1) pathway on CSE-induced PlGF upregulation in human bronchial epithelium (HBE). Reactive Oxygen Species 64-67 mitogen-activated protein kinase 3 Homo sapiens 180-187 27980400-7 2016 These results demonstrate that ROS activation of the MAPK (ERK-1/2)/Egr-1 pathway is a main player in the regulatory mechanism for CSE-induced PlGF production and that the use of an antioxidant could partly abolish these effects. Reactive Oxygen Species 31-34 mitogen-activated protein kinase 3 Homo sapiens 59-66 27698876-0 2016 Eupatilin induces human renal cancer cell apoptosis via ROS-mediated MAPK and PI3K/AKT signaling pathways. Reactive Oxygen Species 56-59 mitogen-activated protein kinase 3 Homo sapiens 69-73 27994507-7 2016 Blocking the ERK1/2 signaling pathway with the MEK inhibitor U0126 and catalpol significantly protected PreOLs from ROS-mediated apoptosis under OGD. Reactive Oxygen Species 116-119 mitogen-activated protein kinase 3 Homo sapiens 13-19 27698876-7 2016 Furthermore, the ROS inhibitor N-acetyl-L-cysteine was able to rescue the MAPK activation and PI3K/AKT inhibition induced by eupatilin. Reactive Oxygen Species 17-20 mitogen-activated protein kinase 3 Homo sapiens 74-78 27698876-8 2016 Taken together, the results of the present study provide evidence that inhibition of eupatilin induces apoptosis in human RCC via ROS-mediated activation of the MAPK signaling pathway and inhibition of the PI3K/AKT signaling pathway. Reactive Oxygen Species 130-133 mitogen-activated protein kinase 3 Homo sapiens 161-165 27564099-10 2016 In conclusion, co-treatment with curcumin and cisplatin synergistically induced apoptosis through ROS-mediated activation of ERK1/2 in bladder cancer. Reactive Oxygen Species 98-101 mitogen-activated protein kinase 3 Homo sapiens 125-131 27393034-10 2016 NOX-derived ROS and MAPKs (Erk1/2 and p38 MAPK) functioned as upstream activators of NF-kappaB and AP-1, respectively. Reactive Oxygen Species 12-15 mitogen-activated protein kinase 3 Homo sapiens 27-33 27564099-0 2016 Curcumin potentiates antitumor activity of cisplatin in bladder cancer cell lines via ROS-mediated activation of ERK1/2. Reactive Oxygen Species 86-89 mitogen-activated protein kinase 3 Homo sapiens 113-119 27155970-14 2016 Taken together, these findings suggest that extracellular AOPP accumulation triggered NOX-dependent ROS production, which activated ERK1/2 and p38 MAPK, and induced HaCaT cell apoptosis by activating caspase 3 and PARP-1. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 3 Homo sapiens 132-138 27313009-6 2016 Moreover, Nox-dependent ROS generation led to phosphorylation of ERK1/2, p38, and JNK, which then activated the downstream molecules NF-kappaB and AP-1, respectively. Reactive Oxygen Species 24-27 mitogen-activated protein kinase 3 Homo sapiens 65-71 27313009-8 2016 Our results reveal for the first time that PMs-induced ROS generation is mediated through the AhR/p47 phox/NADPH oxidase pathway, which in turn activates ERK1/2, p38/NF-kappaB and JNK/AP-1, and which ultimately induces COX2 expression and filaggrin downregulation. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 3 Homo sapiens 154-160 27248323-5 2016 In stark contrast, ERK1/2 was suppressed by ROS and exhibited an inhibitory effect on the differentiation but showed a weak promotion on the expression of extracellular matrix proteins. Reactive Oxygen Species 44-47 mitogen-activated protein kinase 3 Homo sapiens 19-25 27248323-8 2016 Our results suggest a novel ROS-mediated shift of dominance from the inhibitory ERK1/2 to the stimulatory p38, JNK1/2 and Notch3 during the pathological progression of IPF. Reactive Oxygen Species 28-31 mitogen-activated protein kinase 3 Homo sapiens 80-86 26407680-7 2016 Further investigation showed that UCB inhibited reactive oxygen species production, which is involved in the repression of ERK1/2 activation and matrix metalloproteinase-2 (MMP-2) expression. Reactive Oxygen Species 48-71 mitogen-activated protein kinase 3 Homo sapiens 123-129 26906511-0 2016 Folic Acid Attenuates Vascular Endothelial Cell Injury Caused by Hypoxia via the Inhibition of ERK1/2/NOX4/ROS Pathway. Reactive Oxygen Species 107-110 mitogen-activated protein kinase 3 Homo sapiens 95-101 26993595-4 2016 We show that the effects of CO on tumor stroma and reprogramming of macrophages towards the anti-tumoral phenotype is mediated by reactive oxygen species (ROS)-dependent activation of MAPK/Erk1/2-c-myc pathway as well as Notch 1-dependent negative feedback on the metabolic enzyme heme oxygenase-1 (HO-1). Reactive Oxygen Species 130-153 mitogen-activated protein kinase 3 Homo sapiens 189-195 26993595-4 2016 We show that the effects of CO on tumor stroma and reprogramming of macrophages towards the anti-tumoral phenotype is mediated by reactive oxygen species (ROS)-dependent activation of MAPK/Erk1/2-c-myc pathway as well as Notch 1-dependent negative feedback on the metabolic enzyme heme oxygenase-1 (HO-1). Reactive Oxygen Species 155-158 mitogen-activated protein kinase 3 Homo sapiens 189-195 26875562-8 2016 Taken together, our studies indicate that hydrogen prevents AAC-induced vascular hypertrophy in vivo, and inhibits Ang II-induced proliferation and migration of VSMCs in vitro possibly by targeting ROS-dependent ERK1/2, p38 MAPK, JNK and ERM signaling. Reactive Oxygen Species 198-201 mitogen-activated protein kinase 3 Homo sapiens 212-218 26875562-8 2016 Taken together, our studies indicate that hydrogen prevents AAC-induced vascular hypertrophy in vivo, and inhibits Ang II-induced proliferation and migration of VSMCs in vitro possibly by targeting ROS-dependent ERK1/2, p38 MAPK, JNK and ERM signaling. Reactive Oxygen Species 198-201 mitogen-activated protein kinase 3 Homo sapiens 224-228 26906511-14 2016 Taken together, the results suggested that hypoxia decreased the cell survival rate and induced apoptosis via ERK1/2/NOX4/ROS pathway, which could be the target of folic acid in protecting the HUVECs from injury caused by hypoxia. Reactive Oxygen Species 122-125 mitogen-activated protein kinase 3 Homo sapiens 110-116 26871469-9 2016 Further, the inhibitors of ERK1/2, JNK, Akt, and NF-kappaB attenuate XCT-790 induced ROS generation. Reactive Oxygen Species 85-88 mitogen-activated protein kinase 3 Homo sapiens 27-33 26300055-12 2015 ROS increment was responsible for the PKC-alpha activation that provoked EGFR transactivation and consequential phosphorylation of ERK1/2. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 131-137 26472194-7 2015 Importantly, the study also identified the crucial role of reactive oxygen species (ROS)-dependent activation of the extracellular signal-regulated kinase1/2 (ERK1/2) in the facilitation of SNG-induced autophagic cell death. Reactive Oxygen Species 59-82 mitogen-activated protein kinase 3 Homo sapiens 159-165 26472194-7 2015 Importantly, the study also identified the crucial role of reactive oxygen species (ROS)-dependent activation of the extracellular signal-regulated kinase1/2 (ERK1/2) in the facilitation of SNG-induced autophagic cell death. Reactive Oxygen Species 84-87 mitogen-activated protein kinase 3 Homo sapiens 159-165 26084532-0 2016 Early Growth Response Protein-1 Expression by Insulin-Like Growth Factor-1 Requires ROS-Dependent Activation of ERK1/2 and PKB Pathways in Vascular Smooth Muscle Cells. Reactive Oxygen Species 84-87 mitogen-activated protein kinase 3 Homo sapiens 112-118 26084532-9 2016 In summary, these data demonstrate that ROS-dependent activation of ERK1/2/JNK, PI3-K/PKB signaling events play a critical role in IGF-1 induced expression of Egr-1 in VSMC. Reactive Oxygen Species 40-43 mitogen-activated protein kinase 3 Homo sapiens 68-74 26565025-10 2015 Inhibition of either ERK1/2 or mTORC1 did not reduce the TGF-beta1-stimulated increase in Nox4 mRNA level but significantly inhibited total Nox4 expression, ROS generation, and apoptosis induced by TGF-beta1. Reactive Oxygen Species 157-160 mitogen-activated protein kinase 3 Homo sapiens 21-27 26149761-4 2015 These effects are due to the increased production of reactive oxygen species which are responsible, at least in part, for the sustained activation of ERK1/2. Reactive Oxygen Species 53-76 mitogen-activated protein kinase 3 Homo sapiens 150-156 26299281-0 2015 Hydrogen sulfide attenuates doxorubicin-induced cardiotoxicity by inhibiting reactive oxygen species-activated extracellular signal-regulated kinase 1/2 in H9c2 cardiac myocytes. Reactive Oxygen Species 77-100 mitogen-activated protein kinase 3 Homo sapiens 111-150 26299281-5 2015 Exposure of H9c2 cardiac myocytes to DOX upregulated the expression levels of phosphorylated ERK1/2, which had been reduced by pretreatment with NaHS or N-acetyl-L-cysteine, a ROS scavenger. Reactive Oxygen Species 176-179 mitogen-activated protein kinase 3 Homo sapiens 93-99 26299281-8 2015 In conclusion, these findings indicate that H2S attenuates DOX-induced cardiotoxicity by inhibiting ROS-mediated activation of ERK1/2 in H9c2 cardiac myocytes. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 3 Homo sapiens 127-133 26442853-12 2015 Inhibitors of reactive oxygen species and phosphatase and tensin homolog restored AKT phosphorylation but abolished ERK1/2 phosphorylation, suggesting that the reactive oxygen species-dependent increase in phosphatase and tensin homolog activity in reperfusion period relieves ERK1/2 from inhibition of AKT. Reactive Oxygen Species 14-37 mitogen-activated protein kinase 3 Homo sapiens 116-122 26442853-12 2015 Inhibitors of reactive oxygen species and phosphatase and tensin homolog restored AKT phosphorylation but abolished ERK1/2 phosphorylation, suggesting that the reactive oxygen species-dependent increase in phosphatase and tensin homolog activity in reperfusion period relieves ERK1/2 from inhibition of AKT. Reactive Oxygen Species 14-37 mitogen-activated protein kinase 3 Homo sapiens 277-283 26442853-12 2015 Inhibitors of reactive oxygen species and phosphatase and tensin homolog restored AKT phosphorylation but abolished ERK1/2 phosphorylation, suggesting that the reactive oxygen species-dependent increase in phosphatase and tensin homolog activity in reperfusion period relieves ERK1/2 from inhibition of AKT. Reactive Oxygen Species 160-183 mitogen-activated protein kinase 3 Homo sapiens 116-122 26442853-12 2015 Inhibitors of reactive oxygen species and phosphatase and tensin homolog restored AKT phosphorylation but abolished ERK1/2 phosphorylation, suggesting that the reactive oxygen species-dependent increase in phosphatase and tensin homolog activity in reperfusion period relieves ERK1/2 from inhibition of AKT. Reactive Oxygen Species 160-183 mitogen-activated protein kinase 3 Homo sapiens 277-283 26416516-9 2015 Terrein also alleviated reactive oxygen species formation through the Nrf2/HO-1/p-ERK1/2 pathway in aged cells. Reactive Oxygen Species 24-47 mitogen-activated protein kinase 3 Homo sapiens 82-88 25979335-10 2015 Mechanistically, thrombin-induced ERK1/2 activation required NADPH oxidase 2-mediated reactive oxygen species (ROS) production, and reverse-mode NCX inhibitors and NCX1 siRNA suppressed thrombin-induced ROS production. Reactive Oxygen Species 86-109 mitogen-activated protein kinase 3 Homo sapiens 34-40 25979335-10 2015 Mechanistically, thrombin-induced ERK1/2 activation required NADPH oxidase 2-mediated reactive oxygen species (ROS) production, and reverse-mode NCX inhibitors and NCX1 siRNA suppressed thrombin-induced ROS production. Reactive Oxygen Species 111-114 mitogen-activated protein kinase 3 Homo sapiens 34-40 25979335-10 2015 Mechanistically, thrombin-induced ERK1/2 activation required NADPH oxidase 2-mediated reactive oxygen species (ROS) production, and reverse-mode NCX inhibitors and NCX1 siRNA suppressed thrombin-induced ROS production. Reactive Oxygen Species 203-206 mitogen-activated protein kinase 3 Homo sapiens 34-40 25979335-11 2015 We propose that reverse-mode NCX is a novel mechanism contributing to thrombin-induced angiogenesis and hyperpermeability by mediating ERK1/2 activation in a ROS-dependent manner. Reactive Oxygen Species 158-161 mitogen-activated protein kinase 3 Homo sapiens 135-141 25889655-11 2015 CONCLUSIONS: SSc T lymphocityes are characterized by high levels of ROS, generated by NADPH oxidase via ERK1/2 phosphorylation, that are essential for cell activation, proliferation, and cytokine production. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 3 Homo sapiens 104-110 25540919-7 2015 Our results demonstrate that RSV is a potent agent against high glucose-induced EMT in renal tubular cells via inhibition of NADPH oxidase/ROS/ERK1/2 pathway. Reactive Oxygen Species 139-142 mitogen-activated protein kinase 3 Homo sapiens 143-149 25582077-8 2015 Phosphoinositide 3-kinase (PI3K) or Erk1/2 inhibition suppressed PTN-induced ROS production, suggesting that ROS production lays down-stream of PI3K or Erk1/2 activation by PTN. Reactive Oxygen Species 77-80 mitogen-activated protein kinase 3 Homo sapiens 36-42 25582077-8 2015 Phosphoinositide 3-kinase (PI3K) or Erk1/2 inhibition suppressed PTN-induced ROS production, suggesting that ROS production lays down-stream of PI3K or Erk1/2 activation by PTN. Reactive Oxygen Species 77-80 mitogen-activated protein kinase 3 Homo sapiens 152-158 25582077-8 2015 Phosphoinositide 3-kinase (PI3K) or Erk1/2 inhibition suppressed PTN-induced ROS production, suggesting that ROS production lays down-stream of PI3K or Erk1/2 activation by PTN. Reactive Oxygen Species 109-112 mitogen-activated protein kinase 3 Homo sapiens 36-42 25582077-8 2015 Phosphoinositide 3-kinase (PI3K) or Erk1/2 inhibition suppressed PTN-induced ROS production, suggesting that ROS production lays down-stream of PI3K or Erk1/2 activation by PTN. Reactive Oxygen Species 109-112 mitogen-activated protein kinase 3 Homo sapiens 152-158 25582077-10 2015 Collectively, these data suggest that xanthine oxidase-mediated ROS production is required for PTN-induced cell migration through the cell membrane functional complex of alphanubeta3 and RPTPbeta/zeta and activation of c-src, PI3K and ERK1/2 kinases. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 3 Homo sapiens 235-241 25968943-7 2015 We found that fructose caused impairment of glucose utilization and insulin signaling through ROS-mediated activation of JNK and ERK1/2 pathways, which was prevented in the presence of antioxidants. Reactive Oxygen Species 94-97 mitogen-activated protein kinase 3 Homo sapiens 129-135 25445050-9 2015 Results suggest that F015 inhibits palmitate-induced, reactive oxygen species-associated MAPK kinase activation and restored insulin sensitivity through regulating IRS-1 function. Reactive Oxygen Species 54-77 mitogen-activated protein kinase 3 Homo sapiens 89-93 25097229-5 2014 Here, we report that methionyl-tRNA synthetase (MRS) is phosphorylated at Ser209 and Ser825 by extracellular signal-related kinase (ERK1/2) under conditions of stress caused by reactive oxygen species (ROS), and that this phosphorylated MRS shows increased affinity for non-cognate tRNAs with lower affinity for tRNA(Met), leading to an increase in Met residues in cellular proteins. Reactive Oxygen Species 177-200 mitogen-activated protein kinase 3 Homo sapiens 132-138 24963595-0 2014 Verrucarin A induces apoptosis through ROS-mediated EGFR/MAPK/Akt signaling pathways in MDA-MB-231 breast cancer cells. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 3 Homo sapiens 57-61 24818995-9 2014 Moreover, specific inhibition of Erk-1/2, IGF-1R, and FGFR-1 activity promoted ROS generation and this effect was not cumulative with that of insulin alone. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 3 Homo sapiens 33-40 25341041-7 2014 ROS enhanced beta-cell differentiation through modulation of ERK1/2 signaling. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 61-67 25097229-5 2014 Here, we report that methionyl-tRNA synthetase (MRS) is phosphorylated at Ser209 and Ser825 by extracellular signal-related kinase (ERK1/2) under conditions of stress caused by reactive oxygen species (ROS), and that this phosphorylated MRS shows increased affinity for non-cognate tRNAs with lower affinity for tRNA(Met), leading to an increase in Met residues in cellular proteins. Reactive Oxygen Species 202-205 mitogen-activated protein kinase 3 Homo sapiens 132-138 25324778-6 2014 ROS activates inflammasome through mitogen-activated protein kinases (MAPK) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 70-74 25773924-10 2014 Moreover, 15 d-PGJ2 generated reactive oxygen species (ROS), which contribute to the expression of 15-PGDH as well as phosphorylation of ERK1/2 and Elk-1. Reactive Oxygen Species 30-53 mitogen-activated protein kinase 3 Homo sapiens 137-143 25773924-10 2014 Moreover, 15 d-PGJ2 generated reactive oxygen species (ROS), which contribute to the expression of 15-PGDH as well as phosphorylation of ERK1/2 and Elk-1. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 3 Homo sapiens 137-143 25773924-12 2014 Taken together, these findings suggest that 15 d-PGJ2 induces the expression of 15-PGDH through ROS-mediated activation of ERK1/2 and subsequently Elk-1 in the MDA-MB-231 cells, which may contribute to tumor suppressive activity of this cyclopentenone prostaglandin. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 3 Homo sapiens 123-129 25027398-8 2014 Taken together, our results suggest that VA-induces apoptosis and cell cycle deregulation in MCF-7 cells through ROS-dependent p38MAPK activation. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 3 Homo sapiens 130-134 25324778-6 2014 ROS activates inflammasome through mitogen-activated protein kinases (MAPK) and extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 136-142 24113843-11 2014 In turn, reactive oxygen species from NADPH oxidase can stimulate ERK1/2 phosphorylation and activation of cPLA2 and result in a release of arachidonic acid. Reactive Oxygen Species 9-32 mitogen-activated protein kinase 3 Homo sapiens 66-72 24858370-13 2014 The present data show that EMD treatment at the beginning of reperfusion-similarly to IPO- limited infarct size and attenuated the postischemic impairment of myocardial function through reactive oxygen species-mediated ERK1/2/Akt/GSK-3beta/eNOS pathways. Reactive Oxygen Species 186-209 mitogen-activated protein kinase 3 Homo sapiens 219-225 24442713-0 2014 Angiotensin II-derived reactive oxygen species promote angiogenesis in human late endothelial progenitor cells through heme oxygenase-1 via ERK1/2 and AKT/PI3K pathways. Reactive Oxygen Species 23-46 mitogen-activated protein kinase 3 Homo sapiens 140-146 24442713-6 2014 Accordingly, Ang II-derived ROS could promote angiogenesis in late EPCs by inducing HO-1 expression via ERK1/2 and AKT/PI3K pathways, and we believe HO-1 might be a promising intervention target in EPCs due to its potent proangiogenic, antioxidant, and antiapoptosis potentials. Reactive Oxygen Species 28-31 mitogen-activated protein kinase 3 Homo sapiens 104-110 24699005-10 2014 SIGNIFICANCE: Metarhizin A is a potent inhibitor of cytochrome c oxidase and activates the MAPK pathway through the generation of ROS, which induces growth arrest of cells, and, under some conditions, enhances cell death. Reactive Oxygen Species 130-133 mitogen-activated protein kinase 3 Homo sapiens 91-95 24732598-11 2014 Inhibition of ROS production with DPI attenuated DFO-induced ERK1/2 activation. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 3 Homo sapiens 61-67 24277866-10 2014 Taken together, these findings suggest that NO modulates ventricular sarcK(ATP) channels via a novel sGC-cGMP-PKG-ROS(H2O2)-ERK1/2-calmodulin-CaMKII (delta isoform in particular) signalling cascade, which heightens K(ATP) channel activity by destabilizing the long closed states while facilitating closed-to-open state transitions. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 3 Homo sapiens 124-130 24586933-4 2014 We report that inhibitors of ERK1/2 phosphorylation upheld natural killer (NK) cell-mediated cytotoxicity under conditions of oxidative stress and rescued NK cells and CD8(+) T lymphocytes from cell death induced by ROS-producing monocytes. Reactive Oxygen Species 216-219 mitogen-activated protein kinase 3 Homo sapiens 29-35 24586933-5 2014 ERK1/2 phosphorylation inhibition also protected lymphocytes from cell death induced by exogenous hydrogen peroxide (H2O2) and from ROS generated by xanthine oxidase or glucose oxidase. Reactive Oxygen Species 132-135 mitogen-activated protein kinase 3 Homo sapiens 0-6 24586933-6 2014 Phosphorylation of ERK1/2 was observed in lymphocytes shortly after exposure to ROS. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 3 Homo sapiens 19-25 24586933-8 2014 ERK1/2 phosphorylation was induced by ROS independently of PARP-1. Reactive Oxygen Species 38-41 mitogen-activated protein kinase 3 Homo sapiens 0-6 24586933-9 2014 Our findings are suggestive of a role for ERK1/2 in ROS-induced lymphocyte parthanatos, and that the ERK axis may provide a therapeutic target for the protection of lymphocytes against oxidative stress. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 3 Homo sapiens 42-48 24409324-7 2014 In addition, ROS dependent activation of Ras and ERK1/2 Kinase was observed to be mediating the TJP-1 disassembly, and endothelial dysfunction in response to cocaine and Tat exposure. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 3 Homo sapiens 49-55 24409324-8 2014 In conclusion, our findings demonstrate that Tat/cocaine -mediated production of ROS activate Ras/Raf/ERK1/2 pathway that contributes to disruption of tight junction protein leading to pulmonary endothelial dysfunction associated with pulmonary vascular remodeling. Reactive Oxygen Species 81-84 mitogen-activated protein kinase 3 Homo sapiens 102-108 24161842-9 2013 The upregulation appeared largely independent of reactive oxygen species generation or metabolic stress and was mainly under transcriptional control, with ERK1/2 playing an important regulating role in the process. Reactive Oxygen Species 49-72 mitogen-activated protein kinase 3 Homo sapiens 155-161 23666878-11 2013 Quenching of ROS by knockdown of NOX-2 or NOX-4 transcripts inhibited phosphorylation of ERK-1/2 and p38 MAPK. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 3 Homo sapiens 89-96 24026617-3 2013 Furthermore, this complex showed a strong energy-dependent and non-endocytotic uptake and exhibited multiple anti-cancer functions by inhibiting the expressions of p-Akt and p-Erk1/2 proteins and by decreasing the levels of reactive oxygen species. Reactive Oxygen Species 224-247 mitogen-activated protein kinase 3 Homo sapiens 176-182 23994527-5 2013 These findings suggest that DA generates mitochondria-derived ROS that activate ERK1/2 and subsequently NF-kappaB and SOD activity at concentrations that exert a physiological regulation of renal function. Reactive Oxygen Species 62-65 mitogen-activated protein kinase 3 Homo sapiens 80-86 24040019-11 2013 Activation of ROS- dependent JNK played a crucial role in ERK1/2 activation which subsequently induced the expression of inducible nitric oxide synthase (iNOS). Reactive Oxygen Species 14-17 mitogen-activated protein kinase 3 Homo sapiens 58-64 24113386-0 2013 NADPH oxidase subunit p22(phox)-mediated reactive oxygen species contribute to angiogenesis and tumor growth through AKT and ERK1/2 signaling pathways in prostate cancer. Reactive Oxygen Species 41-64 mitogen-activated protein kinase 3 Homo sapiens 125-131 24383372-8 2013 ROS generation in response to TGF-beta1, measured as 2,7-dichlorofluorescein-diacetate fluorescence, was inhibited significantly by SB203580 and U0126, implicating both the p38 MAPK and Mekl/2/Erk1/2 signaling pathways. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 193-199 23666878-12 2013 Moreover, inhibitors of ERK-1/2 and p38 MAPK decreased ROS production and subsequent EPC apoptosis, indicating a feed-forward loop between NOX and MAPK to amplify ROS production related to apoptosis. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 3 Homo sapiens 24-31 23666878-12 2013 Moreover, inhibitors of ERK-1/2 and p38 MAPK decreased ROS production and subsequent EPC apoptosis, indicating a feed-forward loop between NOX and MAPK to amplify ROS production related to apoptosis. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 3 Homo sapiens 40-44 23666878-12 2013 Moreover, inhibitors of ERK-1/2 and p38 MAPK decreased ROS production and subsequent EPC apoptosis, indicating a feed-forward loop between NOX and MAPK to amplify ROS production related to apoptosis. Reactive Oxygen Species 163-166 mitogen-activated protein kinase 3 Homo sapiens 24-31 23666878-12 2013 Moreover, inhibitors of ERK-1/2 and p38 MAPK decreased ROS production and subsequent EPC apoptosis, indicating a feed-forward loop between NOX and MAPK to amplify ROS production related to apoptosis. Reactive Oxygen Species 163-166 mitogen-activated protein kinase 3 Homo sapiens 40-44 23685456-9 2013 We speculated that ROS generation might be the first event of Dex-induced apoptosis because ROS inhibitor NAC abrogated ROS production and ERK1/2 activation, but PD98059 did not block ROS production. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 3 Homo sapiens 139-145 23740244-8 2013 The effect of ROS on NF-kappaB and HIF-1alpha is mediated through activation of ERK1/2 and Akt, and their pharmacological inhibition also suppresses gemcitabine-induced CXCR4 up-regulation. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 3 Homo sapiens 80-86 22664326-9 2012 Our results suggest that ROS stimulated TGF-beta1 secretion and MAPK activation, resulting in EMT initiation in NHEKs. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 3 Homo sapiens 64-68 22688575-3 2013 In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. Reactive Oxygen Species 69-92 mitogen-activated protein kinase 3 Homo sapiens 179-186 22688575-3 2013 In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. Reactive Oxygen Species 94-97 mitogen-activated protein kinase 3 Homo sapiens 179-186 23363008-0 2013 Chicoric acid induces apoptosis in 3T3-L1 preadipocytes through ROS-mediated PI3K/Akt and MAPK signaling pathways. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 3 Homo sapiens 90-94 23750203-6 2013 Functional investigation demonstrated that AL-1 exerted its protective effects on H2O2-induced cell death of beta-cells by generating NADPH oxidase-dependent ROS to activate ERK1/2 and AKT1 signaling pathways. Reactive Oxygen Species 158-161 mitogen-activated protein kinase 3 Homo sapiens 174-180 23263730-9 2013 Consequently, we concluded that intracellular ROS, increased by ionizing radiation, modulate megakaryocytic differentiation downstream of the MAPK pathway. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 3 Homo sapiens 142-146 23314357-9 2013 2,2,6,6-Tetramethyl-1-piperidinyloxy (TEMPO), a ROS scavenger, prevented the phosphorylation of ERK1/2. Reactive Oxygen Species 48-51 mitogen-activated protein kinase 3 Homo sapiens 96-102 23314357-14 2013 Taking the above findings into account, it can be concluded that nutlin-3 activates ERK1/2 prior to EGFR phosphorylation via ROS generation following the mitochondrial translocation of p53 and that nutlin-3-induced ERK1/2 activation may play a role in protecting U2OS cells from p53-dependent apoptosis, constituting a negative feedback loop for p53-induced apoptosis. Reactive Oxygen Species 125-128 mitogen-activated protein kinase 3 Homo sapiens 84-90 22659808-0 2012 Rosiglitazone inhibits angiotensin II-induced C-reactive protein production in human aortic endothelial cells through regulating AT(1)-ROS-MAPK signal pathway. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 3 Homo sapiens 139-143 22728070-0 2012 Reactive oxygen species are required for beta2 adrenergic receptor-beta-arrestin interactions and signaling to ERK1/2. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 3 Homo sapiens 111-117 22728070-7 2012 Using phosphorylation of ERK1/2 as a functional endpoint to assess the role of ROS in beta2AR-beta-arrestin signaling, our results show that inhibition of intracellular ROS abrogates both the beta-arrestin and G protein-mediated phosphorylation of ERK1/2 upon agonism of beta2AR. Reactive Oxygen Species 169-172 mitogen-activated protein kinase 3 Homo sapiens 25-31 22728070-7 2012 Using phosphorylation of ERK1/2 as a functional endpoint to assess the role of ROS in beta2AR-beta-arrestin signaling, our results show that inhibition of intracellular ROS abrogates both the beta-arrestin and G protein-mediated phosphorylation of ERK1/2 upon agonism of beta2AR. Reactive Oxygen Species 169-172 mitogen-activated protein kinase 3 Homo sapiens 248-254 22659808-11 2012 CONCLUSIONS: Rosiglitazone at the concentrations used in the present experiment is able to inhibit Ang II-induced CRP generation in HAECs by regulating AT(1)-ROS-MAPK signal pathway. Reactive Oxygen Species 158-161 mitogen-activated protein kinase 3 Homo sapiens 162-166 21978886-8 2012 In conclusion, these results suggest that salidroside inhibits tumor cells metastasis, which may due to its interfere in the intracellular excess ROS thereby down-regulated the ROS-PKC-ERK1/2 signaling pathway. Reactive Oxygen Species 177-180 mitogen-activated protein kinase 3 Homo sapiens 185-191 22490436-9 2012 This is evidenced by the findings that CPT induced ROS in a concentration- and time-dependent manner; CPT induction of ROS was inhibited by N-acetyl-L-cysteine (NAC), a ROS scavenger; and NAC attenuated CPT activation of p38/JNK, inhibition of Erk1/2, and induction of cell death. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 3 Homo sapiens 244-250 22490436-9 2012 This is evidenced by the findings that CPT induced ROS in a concentration- and time-dependent manner; CPT induction of ROS was inhibited by N-acetyl-L-cysteine (NAC), a ROS scavenger; and NAC attenuated CPT activation of p38/JNK, inhibition of Erk1/2, and induction of cell death. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 3 Homo sapiens 244-250 22490436-10 2012 The results suggested that CPT induction of ROS activates p38/JNK and inhibits Erk1/2, leading to caspase-independent cell death in tumor cells. Reactive Oxygen Species 44-47 mitogen-activated protein kinase 3 Homo sapiens 79-85 22108091-3 2012 Strikingly, telomerase overexpression in normal human fibroblasts treated with TNF-alpha strongly repressed ROS-dependent activation of both ERK1/2 mitogen-activated protein kinases and cell death. Reactive Oxygen Species 108-111 mitogen-activated protein kinase 3 Homo sapiens 141-147 21959987-8 2012 In conclusion, hypoxia-induced migration of HSC/MFs involves an early, mitochondrial-dependent ROS-mediated activation of ERK and JNK, followed by a delayed- and HIF-1alpha-dependent up-regulation and release of VEGF. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 3 Homo sapiens 122-125 22683510-6 2012 In addition, N-acetyl cysteine (NAC), an ROS scavenger, blocked cell cycle G2/M arrest and phosphorylation of ERK1/2 and Cdc25cSer(216) in U87 cells. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 3 Homo sapiens 110-116 22575515-8 2012 Meanwhile, results also showed that N-acetylcysteine (a reactive oxygen species scavenger) suppressed the proliferation and the ERK1/2 and JNK activation induced by 5-HT. Reactive Oxygen Species 56-79 mitogen-activated protein kinase 3 Homo sapiens 128-134 23115616-7 2012 This down-regulatory effect was dependent on the release of reactive oxygen species elicited by 15dPGJ(2), since it was enhanced by pro-oxidant treatment and reversed by antioxidants, and was also mediated by ERK1/2 activation. Reactive Oxygen Species 60-83 mitogen-activated protein kinase 3 Homo sapiens 209-215 22111577-7 2011 Phosphorylation of ERK1/2 and p38 was attenuated using NAC to inhibit ROS production. Reactive Oxygen Species 70-73 mitogen-activated protein kinase 3 Homo sapiens 19-25 22111577-8 2011 After treatment with 1, ROS provided a specific environment that resulted in MAPK-induced cell death, with this effect reduced by the ERK1/2 specific inhibitor PD98059 and partially inhibited by the p38 inhibitor SB203580. Reactive Oxygen Species 24-27 mitogen-activated protein kinase 3 Homo sapiens 134-140 21082355-0 2011 Modulation of ROS/MAPK signaling pathways by okadaic acid leads to cell death via, mitochondrial mediated caspase-dependent mechanism. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 3 Homo sapiens 18-22 21978883-4 2011 In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Abeta42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). Reactive Oxygen Species 165-188 mitogen-activated protein kinase 3 Homo sapiens 324-330 21978883-4 2011 In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Abeta42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). Reactive Oxygen Species 190-193 mitogen-activated protein kinase 3 Homo sapiens 324-330 21978883-7 2011 Ab(RAGE) as well as NADPH oxidase inhibitor and ROS scavenger suppressed Abeta42-induced ERK1/2 and cPLA2 phosphorylation in CECs. Reactive Oxygen Species 48-51 mitogen-activated protein kinase 3 Homo sapiens 89-95 21145826-7 2011 All polypeptides induced a NADPH-oxidase-dependent intracellular rise in ROS, resulting in activation of ERK1/2 and JNK1/2. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 3 Homo sapiens 105-111 20473523-0 2011 Differential induction of reactive oxygen species through Erk1/2 and Nox-1 by FK228 for selective apoptosis of oncogenic H-Ras-expressing human urinary bladder cancer J82 cells. Reactive Oxygen Species 26-49 mitogen-activated protein kinase 3 Homo sapiens 58-64 21056559-9 2011 Furthermore, ROS generation by J774A.1-MacCM is required for Akt and ERK1/2 signaling to promote 3T3-L1 preadipocyte survival. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 3 Homo sapiens 69-75 21123734-6 2011 The ROS-induced CO-mediated survival mechanism requires functional interactions between the protein kinase B/Akt and extracellular signal-related kinase (ERK)/p38 MAPK signaling pathways activated by TNF-alpha. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 3 Homo sapiens 163-167 21123734-9 2011 The ROS-dependent cell survival pathway is mediated by an endogenous antioxidant CO, which inhibits Nox4 activation via a mechanism that includes Akt, ERK1/2, and p38 MAPK signaling pathways. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 3 Homo sapiens 151-157 21123734-9 2011 The ROS-dependent cell survival pathway is mediated by an endogenous antioxidant CO, which inhibits Nox4 activation via a mechanism that includes Akt, ERK1/2, and p38 MAPK signaling pathways. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 3 Homo sapiens 167-171 21123734-10 2011 The ability of CO to inhibit TNF-alpha-induced ERK1/2 and p38 MAPK activities in an Akt-dependent manner appears to be the key element in ROS-dependent survival of endothelial cells during TNF-alpha-mediated brain inflammatory disease. Reactive Oxygen Species 138-141 mitogen-activated protein kinase 3 Homo sapiens 47-53 21800350-7 2011 Our study strongly supports the hypothesis that Lu might protect SH-SY5Y cells against ROS-mediated apoptotic cell death induced by zinc in part by inhibiting the PI3K-Akt-NF-kappaB-ERKs pathway. Reactive Oxygen Species 87-90 mitogen-activated protein kinase 3 Homo sapiens 182-186 21971544-9 2011 We also observed these cells constitutively produce ROS, which was required for the constitutive activation of AKT, ERK1/2, mTOR, and p70S6K1. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 3 Homo sapiens 116-122 21971544-11 2011 These results indicate cell transformation induced by chronic arsenic exposure is mediated by increased cellular levels of ROS, which mediates activation of AKT, ERK1/2, and p70S6K1. Reactive Oxygen Species 123-126 mitogen-activated protein kinase 3 Homo sapiens 162-168 21943001-10 2011 Finally, inhibition of either of these ROS-induced signaling pathways suppressed cytokine (TNF-alpha and IL-1beta) production, while chemokine (CCL2 and CXCL10) induction pathways were sensitive to inhibition of p38, but not ERK1/2 MAPK. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 3 Homo sapiens 225-231 21943001-10 2011 Finally, inhibition of either of these ROS-induced signaling pathways suppressed cytokine (TNF-alpha and IL-1beta) production, while chemokine (CCL2 and CXCL10) induction pathways were sensitive to inhibition of p38, but not ERK1/2 MAPK. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 3 Homo sapiens 232-236 20518705-7 2011 Reintroduction of oxygen generates reactive oxygen species that activate protein kinase C to increase sensitivity of adenosine A(2b) receptors allowing adenosine released from ischemic cells to bind leading to activation of phosphatidylinositol 3-kinase and extracellular signal-regulated kinase 1/2. Reactive Oxygen Species 35-58 mitogen-activated protein kinase 3 Homo sapiens 258-299 20518702-7 2011 The Ca(2+) chelation prevented the ERK1/2 activation, and inhibition of the ERK1/2 phosphorylation decreased mitochondrial fragmentation as well as ROS levels in high-glucose stimulation. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 3 Homo sapiens 76-82 21325823-9 2011 These demonstrate that Ang II is capable of inducing CRP generation in macrophages via AT(1)-ROS-ERK1/2/p38MAPK-NF-kappaB signal pathway, which contributes to better understanding of the proinflammatory and proatherosclerotic actions of Ang II. Reactive Oxygen Species 93-96 mitogen-activated protein kinase 3 Homo sapiens 97-103 21461234-9 2011 However, ROS-dependent activation of ERK1/2 and p38 MAPK, but not JNK, might not be involved in the curcumin-induced autophagy. Reactive Oxygen Species 9-12 mitogen-activated protein kinase 3 Homo sapiens 37-43 21881310-5 2011 In addition, ROS mediate activation of mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, p38, and big MAP kinase 1, in various cells leading to change in gene expressions. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 3 Homo sapiens 80-146 22096572-10 2011 Furthermore, FE-mediated apoptosis was found to involve the generation of reactive oxygen species (ROS), which are responsible for the decrease of DeltaPsim and phosphorylation of JNK, p38, and ERK1/2 kinases. Reactive Oxygen Species 74-97 mitogen-activated protein kinase 3 Homo sapiens 194-200 21687637-5 2011 To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF). Reactive Oxygen Species 96-119 mitogen-activated protein kinase 3 Homo sapiens 162-168 21687637-5 2011 To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF). Reactive Oxygen Species 121-124 mitogen-activated protein kinase 3 Homo sapiens 162-168 22096572-10 2011 Furthermore, FE-mediated apoptosis was found to involve the generation of reactive oxygen species (ROS), which are responsible for the decrease of DeltaPsim and phosphorylation of JNK, p38, and ERK1/2 kinases. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 3 Homo sapiens 194-200 20185286-6 2010 Our further investigation revealed this inhibitory effect on cardiac hypertrophy was mediated by blocking the activation of ROS-dependent ERK1/2, JNK1/2 and AKT signaling pathways. Reactive Oxygen Species 124-127 mitogen-activated protein kinase 3 Homo sapiens 138-144 20570722-3 2010 Therefore, we aimed to analyze the ROS dependence of the induced activation of the Akt/ERK1/2 signaling pathway upon exposure to ultrafine particulate matter (UPM). Reactive Oxygen Species 35-38 mitogen-activated protein kinase 3 Homo sapiens 87-93 20592309-7 2010 Inhibiting ERK1/2 inhibited tyr-P of capacitated boar spermatozoa proteins of 172, 97, and 66 kDa (P <= 0.04); with ROS, this inhibition increased (P < 0.002) and tyr-P of 111 kDa declined (P < 0.028). Reactive Oxygen Species 119-122 mitogen-activated protein kinase 3 Homo sapiens 11-17 20592309-10 2010 ROS affect RAF1, MEK1/2, and ERK1/2 and could influence the sequential events of boar sperm capacitation. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 29-35 21311214-5 2010 In the present work we will consider the pathological changes of ROS and RNS signaling in enzyme/gene regulated processes catalyzed by protein kinases C and B (Akt/B), phosphatidylinositol 3"-kinase (PI3-kinase), extracellular signal-regulated kinase 1/2 (ERK1/2), and some others. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 3 Homo sapiens 256-262 20570727-4 2010 IL-13 stimulates intracellular ROS synthesis within 5min via IL-13Ralpha1-JAK1-STAT6- and IL-13Ralpha2-MEK1/2-ERK1/2-dependent activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-1 (NOX-1). Reactive Oxygen Species 31-34 mitogen-activated protein kinase 3 Homo sapiens 110-116 20570727-5 2010 IL-13-induced ROS generation in turn positively regulates phosphorylation of ERK1/2 and STAT6, yielding a feed forward amplification loop. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 3 Homo sapiens 77-83 20538278-12 2010 CONCLUSIONS: The present study demonstrates that AngII has ability to induce CRP expression in HAECs through AT(1)-ROS-ERK1/2 and JNK-NF-kappaB signal pathway, which strengthens understanding of the proinflammatory and proathroscerotic actions of AngII. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 3 Homo sapiens 119-125 21034561-12 2010 CONCLUSION: The activation of NADPH oxidase by thrombin leads to the production of ROS, which promotes fibroblasts proliferation via activation of the ERK1/2 signaling pathway. Reactive Oxygen Species 83-86 mitogen-activated protein kinase 3 Homo sapiens 151-157 20570722-5 2010 Cell-free as well as intracellular particle-induced ROS generation was assessed and related to the induced Akt and ERK1/2 phosphorylation by inhibiting oxidative stress with catalase, superoxide dismutase, and N-acetylcysteine. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 3 Homo sapiens 115-121 20672248-10 2010 Moreover, PPARgamma in aged HDF cells reduced pro-inflammatory molecules and eliminated the formation of reactive oxygen species (ROS) through the ERK1/2 pathway. Reactive Oxygen Species 105-128 mitogen-activated protein kinase 3 Homo sapiens 147-153 20672248-10 2010 Moreover, PPARgamma in aged HDF cells reduced pro-inflammatory molecules and eliminated the formation of reactive oxygen species (ROS) through the ERK1/2 pathway. Reactive Oxygen Species 130-133 mitogen-activated protein kinase 3 Homo sapiens 147-153 20450227-3 2010 Ligand binding to P2X(7) can stimulate ERK1/2, the transcription factor CREB, enzymes linked to the production of reactive oxygen species and interleukin-1 isoforms, and the formation of a nonspecific pore. Reactive Oxygen Species 114-137 mitogen-activated protein kinase 3 Homo sapiens 39-45 20130591-7 2010 By means of chemical inhibitors of known signaling pathways, we showed that ERK1/2, the p38-, JNK-, PI3K/AKT-, STAT3-, and IL-6 as well as the calcium-mediated signaling pathways, are functionally involved in the IRA gene response and that a major part of it is triggered by mitochondrial and, to a lesser extent, non-mitochondrial production of reactive oxygen species. Reactive Oxygen Species 346-369 mitogen-activated protein kinase 3 Homo sapiens 76-82 19429257-5 2009 Our results show that the Erk1/2 kinases and p38MAPK/JNK are involved in ROS formation in neutrophils exposed to A 1242. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 3 Homo sapiens 26-32 20067818-9 2010 These data suggest that ROS mediated MAPK activation is involved in the molecular mechanisms of BrO(3)(-)-induced cell cycle arrest, which occurs independently of 8-OH-dG production. Reactive Oxygen Species 24-27 mitogen-activated protein kinase 3 Homo sapiens 37-41 19951696-8 2010 The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced. Reactive Oxygen Species 141-144 mitogen-activated protein kinase 3 Homo sapiens 187-193 18941890-2 2009 Reactive oxygen species (ROS) can induce activation of extracellular response kinase 1/2 (Erk1/2) and protein kinase B (Akt). Reactive Oxygen Species 0-23 mitogen-activated protein kinase 3 Homo sapiens 90-96 18941890-2 2009 Reactive oxygen species (ROS) can induce activation of extracellular response kinase 1/2 (Erk1/2) and protein kinase B (Akt). Reactive Oxygen Species 25-28 mitogen-activated protein kinase 3 Homo sapiens 90-96 19709383-7 2009 ROS did not enhance signaling through Smad2 but did enhance activation of p38 and ERK1/2 at 10 min after TGF-beta1. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 82-88 19654295-11 2009 Overall, our results show that zerumbone can potentiate TRAIL-induced apoptosis through the reactive oxygen species-mediated activation of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase leading to DR4 and DR5 induction and resulting in enhancement of the anticancer effects of TRAIL. Reactive Oxygen Species 92-115 mitogen-activated protein kinase 3 Homo sapiens 139-180 19647729-6 2009 We found that apigenin-mediated production of a large amount of intracellular reactive oxygen species (ROS) caused activation of ERK1/2 and apoptosis; treatment with the antioxidant Tiron strongly inhibited the apigenin-induced generation of ROS, phosphorylation of ERK1/2, and apoptotic cell death. Reactive Oxygen Species 78-101 mitogen-activated protein kinase 3 Homo sapiens 129-135 19647729-6 2009 We found that apigenin-mediated production of a large amount of intracellular reactive oxygen species (ROS) caused activation of ERK1/2 and apoptosis; treatment with the antioxidant Tiron strongly inhibited the apigenin-induced generation of ROS, phosphorylation of ERK1/2, and apoptotic cell death. Reactive Oxygen Species 78-101 mitogen-activated protein kinase 3 Homo sapiens 266-272 19647729-6 2009 We found that apigenin-mediated production of a large amount of intracellular reactive oxygen species (ROS) caused activation of ERK1/2 and apoptosis; treatment with the antioxidant Tiron strongly inhibited the apigenin-induced generation of ROS, phosphorylation of ERK1/2, and apoptotic cell death. Reactive Oxygen Species 103-106 mitogen-activated protein kinase 3 Homo sapiens 129-135 19647729-6 2009 We found that apigenin-mediated production of a large amount of intracellular reactive oxygen species (ROS) caused activation of ERK1/2 and apoptosis; treatment with the antioxidant Tiron strongly inhibited the apigenin-induced generation of ROS, phosphorylation of ERK1/2, and apoptotic cell death. Reactive Oxygen Species 103-106 mitogen-activated protein kinase 3 Homo sapiens 266-272 19524565-7 2009 These results indicate that elevated ROS-induced activation of the MAPK signaling pathway could be associated with Cd-induced RPE cell apoptosis, one of the major contributing factors in AMD. Reactive Oxygen Species 37-40 mitogen-activated protein kinase 3 Homo sapiens 67-71 19337723-3 2009 In the present study, we investigated the roles of the ROS-generating Nox4- and Nox2-containing reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases in proliferation of human endothelial cells by examining the impact of these enzyme systems on (1) specific proliferative and tumorigenic kinases, extracellular regulated kinase1/2 (ERK1/2) and Akt, (2) cytoskeletal organization, and (3) the mechanisms that influence cellular apoptosis. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 3 Homo sapiens 347-353 19498006-7 2009 This increase in endogenous ROS correlated with increased cellular proliferation and activation of ERK1/2. Reactive Oxygen Species 28-31 mitogen-activated protein kinase 3 Homo sapiens 99-105 19392662-3 2009 NAD(P)H oxidase-mediated menadione-induced ROS production, which then stimulated phosphorylation of p38 MAPK (mitogen-activated protein kinase) and ERK1/2 (extracellular-signal-regulated kinase 1/2), and increased actin polymerization and cytoskeletal protrusions. Reactive Oxygen Species 43-46 mitogen-activated protein kinase 3 Homo sapiens 148-154 18983479-10 2009 Activation of both ERK1/2 and p38 MAPK is critical for mitochondrial ROS generation. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 3 Homo sapiens 19-25 19318349-8 2009 In summary, PKCalpha, which was activated in senescent cells by ROS strongly activated Erk1/2, and the SA-pErk1/2 in turn phosphorylated Sp1 on Ser(59). Reactive Oxygen Species 64-67 mitogen-activated protein kinase 3 Homo sapiens 87-93 19413885-6 2009 The inhibitory effect of crocetin on cardiac hypertrophy is mediated by blocking the reactive oxygen species (ROS)-dependent mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase-1/2 (MEK/ERK1/2) pathway and GATA binding protein 4 (GATA-4) activation. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 3 Homo sapiens 212-218 19360913-3 2009 ROS participate simultaneously in two signaling pathways that have inverse functions in tumorigenesis, Ras-Raf-MEK1/2-ERK1/2 signaling and the p38 mitogen-activated protein kinases (MAPK) pathway. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 118-124 19360913-3 2009 ROS participate simultaneously in two signaling pathways that have inverse functions in tumorigenesis, Ras-Raf-MEK1/2-ERK1/2 signaling and the p38 mitogen-activated protein kinases (MAPK) pathway. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 3 Homo sapiens 182-186 19054278-8 2009 Interestingly, inhibition of mitogen-activated protein kinase pathway with PD98096 or U0126 caused a decrease in reactive oxygen species production suggesting that activation of ERK1/2 could further exacerbate the oxidative stress caused by glutamate-induced toxicity; however, these inhibitors had no effect on OA-induced toxicity. Reactive Oxygen Species 113-136 mitogen-activated protein kinase 3 Homo sapiens 178-184 19263245-4 2009 We report that P2X(7) stimulates ROS production in macrophages through the MAPKs ERK1/2 and the nicotinamide adenine dinucleotide phosphate oxidase complex, activates several transcription factors including cyclic-AMP response element-binding protein and components of the activating protein-1 complex, and contains specific sequences within its intracellular C-terminus that appear critical for its activity. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 3 Homo sapiens 81-87 19413885-6 2009 The inhibitory effect of crocetin on cardiac hypertrophy is mediated by blocking the reactive oxygen species (ROS)-dependent mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase-1/2 (MEK/ERK1/2) pathway and GATA binding protein 4 (GATA-4) activation. Reactive Oxygen Species 85-108 mitogen-activated protein kinase 3 Homo sapiens 159-163 19413885-6 2009 The inhibitory effect of crocetin on cardiac hypertrophy is mediated by blocking the reactive oxygen species (ROS)-dependent mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase-1/2 (MEK/ERK1/2) pathway and GATA binding protein 4 (GATA-4) activation. Reactive Oxygen Species 85-108 mitogen-activated protein kinase 3 Homo sapiens 212-218 19413885-6 2009 The inhibitory effect of crocetin on cardiac hypertrophy is mediated by blocking the reactive oxygen species (ROS)-dependent mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase-1/2 (MEK/ERK1/2) pathway and GATA binding protein 4 (GATA-4) activation. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 3 Homo sapiens 159-163 18996496-0 2009 Docosahexaenoic acid induces ERK1/2 activation and neuritogenesis via intracellular reactive oxygen species production in human neuroblastoma SH-SY5Y cells. Reactive Oxygen Species 84-107 mitogen-activated protein kinase 3 Homo sapiens 29-35 19172484-0 2009 Vibrio vulnificus-induced cell death of human mononuclear cells requires ROS-dependent activation of p38 and ERK 1/2 MAPKs. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 3 Homo sapiens 109-116 19610261-4 2009 In this study, we investigated the role of mitochondrial ROS in the activation of extracellular signal-regulated kinases (ERK) 1 and 2-mitogen-activated protein kinase (MAPK) and caspase-3 in human eosinophils stimulated with H2O2. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 3 Homo sapiens 169-173 18983479-10 2009 Activation of both ERK1/2 and p38 MAPK is critical for mitochondrial ROS generation. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 3 Homo sapiens 34-38 19014378-9 2008 Furthermore, Asx markedly abolished 6-OHDA-induced reactive oxygen species generation, which resulted in the blockade of p38 MAPK activation and apoptosis induced by 6-OHDA treatment. Reactive Oxygen Species 51-74 mitogen-activated protein kinase 3 Homo sapiens 125-129 19017959-8 2008 These data demonstrate that strategies to decrease mast cell production of ROS and eicosanoids would have to target both ERK1/2- and PI3K/Btk-dependent pathways. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 3 Homo sapiens 121-127 19017959-4 2008 In this study, we demonstrate that, in addition to ERK1/2-dependent pathways, ERK1/2-independent pathways also regulate FcepsilonRI-mediated eicosanoid and ROS production in mast cells. Reactive Oxygen Species 156-159 mitogen-activated protein kinase 3 Homo sapiens 51-57 19017959-4 2008 In this study, we demonstrate that, in addition to ERK1/2-dependent pathways, ERK1/2-independent pathways also regulate FcepsilonRI-mediated eicosanoid and ROS production in mast cells. Reactive Oxygen Species 156-159 mitogen-activated protein kinase 3 Homo sapiens 78-84 18703135-11 2008 The results indicate that Cd induction of ROS inhibits PP2A and PP5, leading to activation of JNK and Erk1/2 pathways, and consequently resulting in caspase-dependent and -independent apoptosis of neuronal cells. Reactive Oxygen Species 42-45 mitogen-activated protein kinase 3 Homo sapiens 102-108 18764868-9 2008 Our results suggest that G-CSF-induced expression of OLFM4 is regulated by the transcription factor NF-kappaB, and that this induction is mediated by the ERK1/2 MAPK signaling pathway through PI3K-driven ROS production. Reactive Oxygen Species 204-207 mitogen-activated protein kinase 3 Homo sapiens 154-160 18764868-9 2008 Our results suggest that G-CSF-induced expression of OLFM4 is regulated by the transcription factor NF-kappaB, and that this induction is mediated by the ERK1/2 MAPK signaling pathway through PI3K-driven ROS production. Reactive Oxygen Species 204-207 mitogen-activated protein kinase 3 Homo sapiens 161-165 18703135-0 2008 Cadmium activates the mitogen-activated protein kinase (MAPK) pathway via induction of reactive oxygen species and inhibition of protein phosphatases 2A and 5. Reactive Oxygen Species 87-110 mitogen-activated protein kinase 3 Homo sapiens 56-60 18703135-6 2008 Furthermore, we found that Cd-induced ROS inhibited serine/threonine protein phosphatases 2A (PP2A) and 5 (PP5), leading to activation of Erk1/2 and JNK, which was abrogated by NAC. Reactive Oxygen Species 38-41 mitogen-activated protein kinase 3 Homo sapiens 138-144 18632752-8 2008 These results suggest a molecular mechanism by which the accumulation of ROS during ovarian cancer progression may cause the degradation of MKP3, which in turn leads to aberrant ERK1/2 activation and contributes to tumorigenicity and chemoresistance of human ovarian cancer cells. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 3 Homo sapiens 178-184 18360712-5 2008 Here we show that mild, but not harsh, heat shock prevented GD-induced necrosis and switched the cell death mode to apoptosis in A549 cells through the ERK1/2 pathway that could suppress GD-induced CuZnSOD release and ROS production. Reactive Oxygen Species 218-221 mitogen-activated protein kinase 3 Homo sapiens 152-158 18270969-0 2008 Redox-regulation of Erk1/2-directed phosphatase by reactive oxygen species: role in signaling TPA-induced growth arrest in ML-1 cells. Reactive Oxygen Species 51-74 mitogen-activated protein kinase 3 Homo sapiens 20-26 18270969-2 2008 Previously, we reported that Erk1/2 activation (phosphorylation) induced by TPA required reactive oxygen species (ROS) as a second messenger. Reactive Oxygen Species 89-112 mitogen-activated protein kinase 3 Homo sapiens 29-35 18270969-2 2008 Previously, we reported that Erk1/2 activation (phosphorylation) induced by TPA required reactive oxygen species (ROS) as a second messenger. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 3 Homo sapiens 29-35 18270969-3 2008 Here, we hypothesized that ROS generated in response to TPA inhibit Erk1/2-directed phosphatase activity, which leads to an increase phosphorylation of Erk1/2 to signal p21(WAF1/Cip1)-mediated growth arrest in ML-1 cells. Reactive Oxygen Species 27-30 mitogen-activated protein kinase 3 Homo sapiens 68-74 18270969-3 2008 Here, we hypothesized that ROS generated in response to TPA inhibit Erk1/2-directed phosphatase activity, which leads to an increase phosphorylation of Erk1/2 to signal p21(WAF1/Cip1)-mediated growth arrest in ML-1 cells. Reactive Oxygen Species 27-30 mitogen-activated protein kinase 3 Homo sapiens 152-158 18270969-8 2008 Together, this study suggested that TPA stimulated ROS generation as a second messenger to activate Erk1/2 via a redox-mediated inhibition of Erk1/2-directed phosphatase in ML-1 cells. Reactive Oxygen Species 51-54 mitogen-activated protein kinase 3 Homo sapiens 100-106 18270969-8 2008 Together, this study suggested that TPA stimulated ROS generation as a second messenger to activate Erk1/2 via a redox-mediated inhibition of Erk1/2-directed phosphatase in ML-1 cells. Reactive Oxygen Species 51-54 mitogen-activated protein kinase 3 Homo sapiens 142-148 18252805-6 2008 Although in tumor cells, curcumin did not significantly affect IR-induced activation of AKT and nuclear factor-kappaB, we found that it caused a significant increase in the production of reactive oxygen species, which further led to sustained extracellular signal-regulated kinase (ERK) 1/2 activation. Reactive Oxygen Species 187-210 mitogen-activated protein kinase 3 Homo sapiens 243-290 17847117-9 2008 These results suggest that the rapid activation of ERK1/2 in dopaminergic cells by oxidative stress serves as a self-protective response, reducing the content of reactive oxygen species and caspase-3 activity and increasing downstream ERK1/2 substrates. Reactive Oxygen Species 162-185 mitogen-activated protein kinase 3 Homo sapiens 51-57 18222975-7 2008 Further studies showed that propofol inhibited the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and mitogen-activated protein kinase/ERK kinase 1/2 (MEK1/2) induced by Ang II via a decrease in ROS production. Reactive Oxygen Species 218-221 mitogen-activated protein kinase 3 Homo sapiens 113-119 17967787-0 2008 Hemin upregulates Egr-1 expression in vascular smooth muscle cells via reactive oxygen species ERK-1/2-Elk-1 and NF-kappaB. Reactive Oxygen Species 71-94 mitogen-activated protein kinase 3 Homo sapiens 95-102 17847117-6 2008 Inhibition of the early phosphorylated ERK1/2 peak with U0126 increased the generation of reactive oxygen species by 6-OHDA as well as 6-OHDA-induced toxicity, whereas inhibition of the late peak did not affect 6-OHDA-induced cell death. Reactive Oxygen Species 90-113 mitogen-activated protein kinase 3 Homo sapiens 39-45 18836276-2 2008 OBJECTIVE: The objective of this study was to investigate the role of the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in the signalling pathway of the novel protein kinase C (PKC)- and reactive oxygen species (ROS)-dependent stimulation of intracellular adenosine 3",5"-cyclic monophosphate (cAMP) production in human eosinophils. Reactive Oxygen Species 205-228 mitogen-activated protein kinase 3 Homo sapiens 130-136 18836276-2 2008 OBJECTIVE: The objective of this study was to investigate the role of the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) in the signalling pathway of the novel protein kinase C (PKC)- and reactive oxygen species (ROS)-dependent stimulation of intracellular adenosine 3",5"-cyclic monophosphate (cAMP) production in human eosinophils. Reactive Oxygen Species 230-233 mitogen-activated protein kinase 3 Homo sapiens 130-136 18836276-9 2008 CONCLUSION: These results reveal the involvement of ERK1/2 in the signalling mechanism of PMA-stimulated, PKC- and ROS-dependent stimulation of cAMP production in human eosinophils, and show that ERK1/2 phosphorylation is upstream of ROS production in the signalling pathway. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 3 Homo sapiens 52-58 18836276-9 2008 CONCLUSION: These results reveal the involvement of ERK1/2 in the signalling mechanism of PMA-stimulated, PKC- and ROS-dependent stimulation of cAMP production in human eosinophils, and show that ERK1/2 phosphorylation is upstream of ROS production in the signalling pathway. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 3 Homo sapiens 196-202 18836276-9 2008 CONCLUSION: These results reveal the involvement of ERK1/2 in the signalling mechanism of PMA-stimulated, PKC- and ROS-dependent stimulation of cAMP production in human eosinophils, and show that ERK1/2 phosphorylation is upstream of ROS production in the signalling pathway. Reactive Oxygen Species 234-237 mitogen-activated protein kinase 3 Homo sapiens 52-58 18836276-9 2008 CONCLUSION: These results reveal the involvement of ERK1/2 in the signalling mechanism of PMA-stimulated, PKC- and ROS-dependent stimulation of cAMP production in human eosinophils, and show that ERK1/2 phosphorylation is upstream of ROS production in the signalling pathway. Reactive Oxygen Species 234-237 mitogen-activated protein kinase 3 Homo sapiens 196-202