PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10764657-12 2000 The results indicate that in VSMCs, Ang II activates MAP kinases and AP-1 through different pathways; the results further suggest that ROS, generated by p22phox, mediate Ang II-induced JNK and p38 MAPK activation, which may contribute to the pathogenesis of atherosclerosis. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 8 Rattus norvegicus 185-188 10807739-3 2000 Thus, the present study aimed to assess the role of ROS in ET-1-mediated activation of c-Jun amino-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) 1/2. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Rattus norvegicus 116-119 10807739-6 2000 JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS. Reactive Oxygen Species 272-275 mitogen-activated protein kinase 8 Rattus norvegicus 0-3 10807739-6 2000 JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS. Reactive Oxygen Species 272-275 mitogen-activated protein kinase 8 Rattus norvegicus 122-125 10807739-8 2000 It was mainly composed of the JNK substrate c-Jun, and activation was also dependent on ROS formation. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 8 Rattus norvegicus 30-33 11075992-7 2000 Whereas CCK-induced activation of MAPK or JNK was totally or partially blocked by protein kinase C (PKC) inhibitor GF-109203X, ROS-induced activation of MAPK, JNK, and p38 MAPK was PKC independent. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Rattus norvegicus 42-45 11075992-7 2000 Whereas CCK-induced activation of MAPK or JNK was totally or partially blocked by protein kinase C (PKC) inhibitor GF-109203X, ROS-induced activation of MAPK, JNK, and p38 MAPK was PKC independent. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Rattus norvegicus 159-162 11075992-8 2000 In conclusion, ROS strongly activate MAPK, JNK, and p38 MAPK in pancreatic acinar cells. Reactive Oxygen Species 15-18 mitogen-activated protein kinase 8 Rattus norvegicus 43-46 34109428-3 2021 The present study hypothesized that the reactive oxygen species (ROS)-mediated JNK signaling pathway may be associated with the protective effect of DHA against MeHg-induced PC12 cell apoptosis. Reactive Oxygen Species 40-63 mitogen-activated protein kinase 8 Rattus norvegicus 79-82 34435888-7 2022 Calcium aggravates renal oxidative stress injury and crystal deposition by activating the Nox4-related reactive oxygen species (ROS)-ERK/JNK pathway in the rat kidney. Reactive Oxygen Species 103-126 mitogen-activated protein kinase 8 Rattus norvegicus 137-140 34435888-7 2022 Calcium aggravates renal oxidative stress injury and crystal deposition by activating the Nox4-related reactive oxygen species (ROS)-ERK/JNK pathway in the rat kidney. Reactive Oxygen Species 128-131 mitogen-activated protein kinase 8 Rattus norvegicus 137-140 34109428-3 2021 The present study hypothesized that the reactive oxygen species (ROS)-mediated JNK signaling pathway may be associated with the protective effect of DHA against MeHg-induced PC12 cell apoptosis. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 8 Rattus norvegicus 79-82 34109428-11 2021 Based on the aforementioned results, the present study indicated that the effects of DHA against MeHg-induced PC12 cell apoptosis may be mediated via the ROS/JNK signaling pathway. Reactive Oxygen Species 154-157 mitogen-activated protein kinase 8 Rattus norvegicus 158-161 32856499-11 2020 In conclusion, CdCl2 induces hippocampal ROS generation and apoptosis by promoting the JNK-mediated activation of p66Shc. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 8 Rattus norvegicus 87-90 34367464-10 2021 In conclusion, we provide mechanistic evidence that AOPPs may induce cell cycle arrest in granulosa cells via the ROS-JNK/p38 MAPK-p21 pathway and thus may be a novel biomarker of POI. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Rattus norvegicus 118-121 35114838-12 2022 Mechanistically, ApoEVs promoted new bone formation by increasing intracellular reactive oxygen species to activate JNK signaling. Reactive Oxygen Species 80-103 mitogen-activated protein kinase 8 Rattus norvegicus 116-119 35270009-12 2022 Collectively, these findings demonstrate that the induction of ROS-activated JNK signaling is a crucial mechanism underlying MeHg-induced mitochondria- and ER stress-dependent apoptosis, ultimately leading to beta-cell death. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 8 Rattus norvegicus 77-80 35527005-0 2022 Dexmedetomidine attenuates acute stress-induced liver injury in rats by regulating the miR-34a-5p/ROS/JNK/p38 signaling pathway. Reactive Oxygen Species 98-101 mitogen-activated protein kinase 8 Rattus norvegicus 102-105 33603672-13 2021 Ga and the JNK inhibitor, sp600125, markedly suppressed Px-12-induced generation of intracellular ROS and O2 -. Reactive Oxygen Species 98-101 mitogen-activated protein kinase 8 Rattus norvegicus 11-14 32948194-5 2020 We concluded that autophagic cell death, resulting from zinc ions-ROS-c-Jun N-terminal kinase (JNK)-autophagy positive feedback loop and blockade of autophagosomal-lysosomal fusion, played a major role in the neurotoxicity of ZnO NPs. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Rattus norvegicus 95-98 32180463-9 2021 And the involvement of JNK pathway was in different mechanism of action that when inhibited leaded to increased cell death, increased generation of ROS but decreased autophagy.Conclusions: These results show a new regulatory mechanism involving ROS-mediated autophagy in rat NP cells, which may provide ideas for drug development to improve compression stress-induced IVDD and help avoid eventual surgical treatment of IVD herniation. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Rattus norvegicus 23-26 32180463-9 2021 And the involvement of JNK pathway was in different mechanism of action that when inhibited leaded to increased cell death, increased generation of ROS but decreased autophagy.Conclusions: These results show a new regulatory mechanism involving ROS-mediated autophagy in rat NP cells, which may provide ideas for drug development to improve compression stress-induced IVDD and help avoid eventual surgical treatment of IVD herniation. Reactive Oxygen Species 245-248 mitogen-activated protein kinase 8 Rattus norvegicus 23-26 32810585-0 2020 Lycopene ameliorates chronic stress-induced hippocampal injury and subsequent learning and memory dysfunction through inhibiting ROS/JNK signaling pathway in rats. Reactive Oxygen Species 129-132 mitogen-activated protein kinase 8 Rattus norvegicus 133-136 32810585-11 2020 Further investigation of the underlying mechanisms revealed that the ROS scavenger N-acetyl-l-cysteine inhibited CRS-induced JNK activation. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 8 Rattus norvegicus 125-128 32428522-12 2020 Low level of ROS may activate JNK signaling pathway and upregulate pro-neuroangiogenic factors, ultimately mediating endothelial angiogenesis. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Rattus norvegicus 30-33 32428522-0 2020 Activation of NADPH/ROS pathway contributes to angiogenesis through JNK signaling in brain endothelial cells. Reactive Oxygen Species 20-23 mitogen-activated protein kinase 8 Rattus norvegicus 68-71 32498294-6 2020 Nox-dependent ROS generation led to phosphorylation of ERK1/2, p38 and JNK, followed by downregulation of microRNA-137. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Rattus norvegicus 71-74 31358627-6 2019 Our results suggest that aberrant Wnt7b expression activated c-jun N-terminal kinase (JNK), which down-regulated mitochondria numbers by suppressing Ppargc1a Down-regulation of Ppargc1a probably decreased reactive oxygen species and enhanced glycolysis. Reactive Oxygen Species 205-228 mitogen-activated protein kinase 8 Rattus norvegicus 61-84 31862514-7 2020 Furthermore, ERK inhibitor (SCH772984), JNK inhibitor (SP600125) and p38 MAPK inhibitor (SB203580) obviously up-regulated BTB-related proteins expression as well as activated Nrf2 expression at varying degrees, indicating that ROS-MAPKs-Nrf2 is involved in the signaling pathway that leads to PM2.5-induced spermatogenesis dysfunction. Reactive Oxygen Species 227-230 mitogen-activated protein kinase 8 Rattus norvegicus 40-43 31519469-2 2019 This study explored the potential role of cJun-N-terminal kinases (JNK) in appetite control, mediated by reactive oxygen species (ROS) and activator protein-1 (AP-1) in AMPH-treated rats. Reactive Oxygen Species 105-128 mitogen-activated protein kinase 8 Rattus norvegicus 67-70 31519469-2 2019 This study explored the potential role of cJun-N-terminal kinases (JNK) in appetite control, mediated by reactive oxygen species (ROS) and activator protein-1 (AP-1) in AMPH-treated rats. Reactive Oxygen Species 130-133 mitogen-activated protein kinase 8 Rattus norvegicus 67-70 31358627-6 2019 Our results suggest that aberrant Wnt7b expression activated c-jun N-terminal kinase (JNK), which down-regulated mitochondria numbers by suppressing Ppargc1a Down-regulation of Ppargc1a probably decreased reactive oxygen species and enhanced glycolysis. Reactive Oxygen Species 205-228 mitogen-activated protein kinase 8 Rattus norvegicus 86-89 30617363-0 2019 Lanthanum chloride induces autophagy in rat hippocampus through ROS-mediated JNK and AKT/mTOR signaling pathways. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Rattus norvegicus 77-80 31205589-0 2019 N-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by Hypoxia/Reoxygenation through the Mitochondrial c-Jun N-Terminal Kinase/Sab/Src/Reactive Oxygen Species Pathway in H9c2 Cells. Reactive Oxygen Species 165-188 mitogen-activated protein kinase 8 Rattus norvegicus 133-156 29467841-13 2018 MFA has anti-oxidant, anti-inflammatory and anti-apoptotic activities and was able to modulate the NOX4/p22phox/ROS-JNK/p38 MAPK signaling pathway. Reactive Oxygen Species 112-115 mitogen-activated protein kinase 8 Rattus norvegicus 116-119 30991755-7 2019 Also, mitochondrial function was improved through the reduced production of ROS and damage of mitochondrial membrane potential (MMP) by regulating the Abeta-related c-Jun N-terminal kinase (JNK)/protein kinase B (Akt) and Akt/apoptosis pathways. Reactive Oxygen Species 76-79 mitogen-activated protein kinase 8 Rattus norvegicus 151-194 30250633-0 2018 Dexmedetomidine Ameliorates Acute Stress-Induced Kidney Injury by Attenuating Oxidative Stress and Apoptosis through Inhibition of the ROS/JNK Signaling Pathway. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 8 Rattus norvegicus 139-142 30250633-12 2018 In summary, DEX protects against acute stress-induced kidney injury in rats by reducing oxidative stress and apoptosis via inhibition of the ROS/JNK pathway. Reactive Oxygen Species 141-144 mitogen-activated protein kinase 8 Rattus norvegicus 145-148 28129433-8 2017 Furthermore, we noticed that expression of wild-type PP5 or dominant negative c-Jun, or pretreatment with JNK inhibitor SP600125 reinforced celastrol"s suppression of Cd-induced NOX2 and its regulatory proteins, and consequential ROS in neuronal cells. Reactive Oxygen Species 230-233 mitogen-activated protein kinase 8 Rattus norvegicus 106-109 28678856-5 2017 Dox administration to cardiomyocytes increased the levels of ROS in a time-dependent manner that followed the activation of stress-induced proteins p53, p38 and JNK MAPKs, culminating in an increase in autophagy and apoptosis markers. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 8 Rattus norvegicus 161-164 27859591-5 2017 Using siRNAs, p38, JNK, PKCalpha, and PKCdelta, as well as ROS scavengers, it was observed that the dependence of PKCalpha/PKCdelta on ROS production to enhance JNK and p38 phosphorylation mediated HG-induced cardiac Nrf2 expression and activation. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 8 Rattus norvegicus 161-164 27859591-8 2017 Our study demonstrated that HG-induced cardiac Nrf2 activation occurs through PKCalpha/PKCdelta-ROS-JNK/p38 signaling. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 8 Rattus norvegicus 100-103 28590722-7 2017 Moreover, they can suppress the oxidative stress damage of BADSCs and improve their survival capacity under ROS microenvironment via activating the ERK and p38 pathways while inhibiting JNK pathway. Reactive Oxygen Species 108-111 mitogen-activated protein kinase 8 Rattus norvegicus 186-189 28129433-9 2017 These findings indicate that celastrol ameliorates Cd-induced neuronal apoptosis via targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. Reactive Oxygen Species 108-111 mitogen-activated protein kinase 8 Rattus norvegicus 126-129 29315209-11 2018 Together, it appears that Pin leads to apoptosis in HSC-T6 cells through ROS-mediated ERK/JNK signaling and caspase-3 activation. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Rattus norvegicus 90-93 28822073-7 2017 IRN blocks the generation of reactive oxygen species upstream of both ASK1/JNK pathway and IRE1/caspase-12 pathway. Reactive Oxygen Species 29-52 mitogen-activated protein kinase 8 Rattus norvegicus 75-78 28656249-8 2017 Furthermore, ROS, and activation of p38, JNK and c-Jun, were revealed to serve pro-apoptosis roles which aggravated damage to epithelial barrier integrity, as assessed by flow cytometry using Annexin V-fluorescein isothiocyanate staining and pretreatment of cells with specific inhibitors of ROS, JNK, p38 and c-Jun (BHA, SP600125, SB203580 and c-Jun peptide, respectively). Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Rattus norvegicus 297-300 28674486-13 2017 Taken together, these findings suggest that AOPPs cause pain hypersensitivity in rats, and extracellular AOPPs accumulation triggered Nox4-dependent ROS production, which activated JNK, and induced DRG neurons apoptosis by activating caspase 3 and PARP-1. Reactive Oxygen Species 149-152 mitogen-activated protein kinase 8 Rattus norvegicus 181-184 28129433-0 2017 Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 8 Rattus norvegicus 96-99 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Reactive Oxygen Species 136-139 mitogen-activated protein kinase 8 Rattus norvegicus 55-78 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Reactive Oxygen Species 136-139 mitogen-activated protein kinase 8 Rattus norvegicus 80-83 28129433-3 2017 Therefore, we hypothesized that celastrol could hinder Cd induction of ROS-dependent PP5-JNK signaling pathway from apoptosis in neuronal cells. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Rattus norvegicus 89-92 25647547-0 2015 Icariin protects H9c2 cardiomyocytes from lipopolysaccharide-induced injury via inhibition of the reactive oxygen species-dependent c-Jun N-terminal kinases/nuclear factor-kappaB pathway. Reactive Oxygen Species 98-121 mitogen-activated protein kinase 8 Rattus norvegicus 132-156 27989749-10 2016 Besides, we found that c-Jun N-terminal kinase1/2 (JNK1/2) was a downstream signaling molecule of ROS that mediated the induction of autophagy by DHA. Reactive Oxygen Species 98-101 mitogen-activated protein kinase 8 Rattus norvegicus 23-49 26195352-6 2015 Moreover, through the application of NOX and JNK inhibitors as well as benzylamine it is shown that the observed response is mediated by reactive oxygen species (ROS), suggesting that miR-15a, miR-15b and miR-16 are novel redoximiRs. Reactive Oxygen Species 137-160 mitogen-activated protein kinase 8 Rattus norvegicus 45-48 26195352-6 2015 Moreover, through the application of NOX and JNK inhibitors as well as benzylamine it is shown that the observed response is mediated by reactive oxygen species (ROS), suggesting that miR-15a, miR-15b and miR-16 are novel redoximiRs. Reactive Oxygen Species 162-165 mitogen-activated protein kinase 8 Rattus norvegicus 45-48 26134032-9 2015 Therefore, H/R activates ROS/Egr-1 signaling pathway in H9c2 cells, and JNK activation plays an important role in this pathway. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Rattus norvegicus 72-75 25915446-12 2015 Further, it was observed that rhein-induced ROS generation is also involved in the modulation of signaling molecules like MAPK kinases, including ERK1/2, p38, and JNK, and mitochondrial energetics proteins, including complexes II-V, p-AMPK, and Sirt-1. Reactive Oxygen Species 44-47 mitogen-activated protein kinase 8 Rattus norvegicus 163-166 25647547-9 2015 These results suggested that icariin prevented cardiomyocytes from inflammatory response and apoptosis, and that this effect may be mediated by inhibition of the ROS-dependent JNK/NF-kappaB pathway. Reactive Oxygen Species 162-165 mitogen-activated protein kinase 8 Rattus norvegicus 176-179 25681429-8 2015 The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP. Reactive Oxygen Species 4-27 mitogen-activated protein kinase 8 Rattus norvegicus 146-149 25769956-7 2015 Pretreatment with the ROS inhibitor N-acetylcysteine abrogated the phosphorylation of p38 and JNK induced by high glucose. Reactive Oxygen Species 22-25 mitogen-activated protein kinase 8 Rattus norvegicus 94-97 25681429-8 2015 The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 8 Rattus norvegicus 146-149 26491537-8 2015 Together, the beneficial effects of allopurinol reducing ROS production may be mediated by normalizing the activity of the ERK, JNK, and Bax/Bcl-2 pathways and by controlling TNF-alpha expression. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 8 Rattus norvegicus 128-131 26021285-7 2015 CONCLUSION: Taken together, our results suggest that administration of EGb761 can ameliorate neuropathic pain, and further indicate that JNK, which is activated by both exogenous and endogenous ROS, might be the mechanism underlying the effects of EGb761 on CCI neuropathic pain. Reactive Oxygen Species 194-197 mitogen-activated protein kinase 8 Rattus norvegicus 137-140 24289330-8 2014 RESULTS: In vivo IFN-alpha2b treatment induced endogenous production of ROS which activated JNK. Reactive Oxygen Species 72-75 mitogen-activated protein kinase 8 Rattus norvegicus 92-95 24960051-4 2014 LPC and GCR inhibited MPP+-induced JNK activation through the suppression of reactive oxygen species (ROS) generation, thereby inhibiting MPP+-induced neuronal PC12D cell death. Reactive Oxygen Species 77-100 mitogen-activated protein kinase 8 Rattus norvegicus 35-38 24960051-4 2014 LPC and GCR inhibited MPP+-induced JNK activation through the suppression of reactive oxygen species (ROS) generation, thereby inhibiting MPP+-induced neuronal PC12D cell death. Reactive Oxygen Species 102-105 mitogen-activated protein kinase 8 Rattus norvegicus 35-38 24294888-7 2014 Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. Reactive Oxygen Species 201-204 mitogen-activated protein kinase 8 Rattus norvegicus 13-16 24940396-0 2014 Icariin attenuates angiotensin II-induced hypertrophy and apoptosis in H9c2 cardiomyocytes by inhibiting reactive oxygen species-dependent JNK and p38 pathways. Reactive Oxygen Species 105-128 mitogen-activated protein kinase 8 Rattus norvegicus 139-142 24940396-9 2014 Therefore, the results of the present study indicated that icariin protected H9c2 cardiomyocytes from Ang II-induced hypertrophy and apoptosis by inhibiting the ROS-dependent JNK and p38 pathways. Reactive Oxygen Species 161-164 mitogen-activated protein kinase 8 Rattus norvegicus 175-178 24294888-12 2014 Taken together, our results suggest that cell death of motor neurons after SCI is mediated through oxidative stress and ER stress-mediated cytochrome c release and VPA-inhibited cytochrome c release by attenuating ROS-induced JNK activation followed by Mcl-1 and Bim phosphorylation and ER stress-coupled CHOP expression. Reactive Oxygen Species 214-217 mitogen-activated protein kinase 8 Rattus norvegicus 226-229 23969109-0 2013 Heme oxygenase-1 induction by the ROS-JNK pathway plays a role in aluminum-induced anemia. Reactive Oxygen Species 34-37 mitogen-activated protein kinase 8 Rattus norvegicus 38-41 24294888-7 2014 Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. Reactive Oxygen Species 89-112 mitogen-activated protein kinase 8 Rattus norvegicus 13-16 24294888-7 2014 Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. Reactive Oxygen Species 89-112 mitogen-activated protein kinase 8 Rattus norvegicus 262-265 24294888-7 2014 Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Rattus norvegicus 13-16 24294888-7 2014 Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Rattus norvegicus 262-265 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 27-50 mitogen-activated protein kinase 8 Rattus norvegicus 80-103 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 27-50 mitogen-activated protein kinase 8 Rattus norvegicus 105-108 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 27-50 mitogen-activated protein kinase 8 Rattus norvegicus 176-179 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Rattus norvegicus 80-103 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Rattus norvegicus 105-108 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Rattus norvegicus 176-179 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 157-160 mitogen-activated protein kinase 8 Rattus norvegicus 80-103 23969109-7 2013 Furthermore, we found that reactive oxygen species (ROS)-mediated activation of c-Jun N-terminal kinase (JNK) was critical for HO-1 induction by Al, because ROS scavengers and JNK inhibitors abrogated enhancement of HO-1 by Al in rat hepatocytes. Reactive Oxygen Species 157-160 mitogen-activated protein kinase 8 Rattus norvegicus 105-108 23969109-8 2013 Thus, Al enhances HO-1 expression through the ROS-JNK pathway, which may enhance HO activity and accelerate degradation of heme, leading to hypochromic anemia. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Rattus norvegicus 50-53 23158927-3 2013 In our previous study, we showed that NADPH oxidase-related ROS-induced apoptosis is mediated via the JNK-dependent activation of NF-kappaB in cardiomyocytes exposed to high glucose (HG). Reactive Oxygen Species 60-63 mitogen-activated protein kinase 8 Rattus norvegicus 102-105 23611574-1 2013 OBJECTIVES: To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats. Reactive Oxygen Species 49-72 mitogen-activated protein kinase 8 Rattus norvegicus 108-129 23611574-1 2013 OBJECTIVES: To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats. Reactive Oxygen Species 49-72 mitogen-activated protein kinase 8 Rattus norvegicus 131-134 23611574-1 2013 OBJECTIVES: To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Rattus norvegicus 108-129 23611574-1 2013 OBJECTIVES: To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Rattus norvegicus 131-134 23258542-1 2013 To build upon recent findings that mitochondrial JNK signaling is inhibited by selectively blocking the interaction between JNK and Sab, we utilized a cell-permeable peptide to demonstrate that ischemia/reperfusion (I/R) injury could be protected in vivo and that JNK mitochondrial signaling was the mechanism by which reactive oxygen species (ROS) generation, mitochondrial dysfunction, and cardiomyocyte cell death occur. Reactive Oxygen Species 319-342 mitogen-activated protein kinase 8 Rattus norvegicus 49-52 23258542-1 2013 To build upon recent findings that mitochondrial JNK signaling is inhibited by selectively blocking the interaction between JNK and Sab, we utilized a cell-permeable peptide to demonstrate that ischemia/reperfusion (I/R) injury could be protected in vivo and that JNK mitochondrial signaling was the mechanism by which reactive oxygen species (ROS) generation, mitochondrial dysfunction, and cardiomyocyte cell death occur. Reactive Oxygen Species 344-347 mitogen-activated protein kinase 8 Rattus norvegicus 49-52 23258542-4 2013 These data suggest that blocking JNK mitochondrial translocation or JNK inhibition prevents ROS increases and mitochondrial dysfunction and may be an effective treatment for I/R-induced cardiomyocyte death. Reactive Oxygen Species 92-95 mitogen-activated protein kinase 8 Rattus norvegicus 33-36 23258542-4 2013 These data suggest that blocking JNK mitochondrial translocation or JNK inhibition prevents ROS increases and mitochondrial dysfunction and may be an effective treatment for I/R-induced cardiomyocyte death. Reactive Oxygen Species 92-95 mitogen-activated protein kinase 8 Rattus norvegicus 68-71 22362362-7 2012 Notably, these cells also exhibited an increase in the activity of the ROS-phospho-JNK (p-JNK)-p-IRS1 (Ser307) axis. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Rattus norvegicus 83-86 23271287-12 2012 The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Rattus norvegicus 64-67 23271287-12 2012 The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Rattus norvegicus 192-195 23271287-14 2012 In conclusion, our results suggest that JNK and ERK1/2 signal pathways, which are activated via ROS, play a crucial role in neuronal apoptosis induced by oxidative stress. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 8 Rattus norvegicus 40-43 22362362-7 2012 Notably, these cells also exhibited an increase in the activity of the ROS-phospho-JNK (p-JNK)-p-IRS1 (Ser307) axis. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Rattus norvegicus 90-93 21077940-12 2011 These findings suggested that ROS mediated ox-LDL-induced LOX-1 expression in VSMCs through NF-kappaB and JNK signaling pathways. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Rattus norvegicus 106-109 22245600-0 2012 High glucose induces renal mesangial cell proliferation and fibronectin expression through JNK/NF-kappaB/NADPH oxidase/ROS pathway, which is inhibited by resveratrol. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 8 Rattus norvegicus 91-94 22245600-8 2012 Mechanistic studies revealed that HG upregulated NADPH oxidase subunits p22(phox) and p47(phox) expression through JNK/NF-kappaB pathway, which resulted in elevation of NADPH oxidase activity and consequent ROS production. Reactive Oxygen Species 207-210 mitogen-activated protein kinase 8 Rattus norvegicus 115-118 22245600-10 2012 These results demonstrate that HG enhances mesangial cell proliferation and fibronectin expression through JNK/NF-kappaB/NADPH oxidase/ROS pathway, which was inhibited by resveratrol. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 8 Rattus norvegicus 107-110 21604272-9 2012 Therefore, we propose that NADPH oxidase-derived ROS-induced apoptosis is mediated via the JNK-dependent activation of NF-kappaB in cardiomyocytes exposed to high glucose. Reactive Oxygen Species 49-52 mitogen-activated protein kinase 8 Rattus norvegicus 91-94 21600974-8 2011 Our data suggest that carmustine-induced neurotoxicity is, at least in part, due to the activation of ROS-dependent JNK and ERK signaling. Reactive Oxygen Species 102-105 mitogen-activated protein kinase 8 Rattus norvegicus 116-119 20863874-8 2010 It is suggested from our results that reactive oxygen species (ROS) have a mediation effect to oxidative stress and up-regulation of JNK and P53 phosphorylation involved in mechanistic pathways of TiO(2)-NPs can induce apoptosis and cell cycle arrest in PC12 cells. Reactive Oxygen Species 38-61 mitogen-activated protein kinase 8 Rattus norvegicus 133-136 20486760-5 2010 NADPH oxidase (Nox)-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 molecules NF-kappaB and c-Jun, respectively. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Rattus norvegicus 121-144 20486760-5 2010 NADPH oxidase (Nox)-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 molecules NF-kappaB and c-Jun, respectively. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Rattus norvegicus 146-149 20486760-8 2010 Taken together, these results suggested that in RBA-1 cells, activation of ERK/NF-kappaB and JNK/c-Jun cascades by a Nox/ROS-dependent event enhancing c-Fos/AP-1 activity is essential for HO-1 upregulation and activation induced by BK. Reactive Oxygen Species 121-124 mitogen-activated protein kinase 8 Rattus norvegicus 93-96 21134288-0 2010 Transforming growth factor-beta1 induces matrix metalloproteinase-9 and cell migration in astrocytes: roles of ROS-dependent ERK- and JNK-NF-kappaB pathways. Reactive Oxygen Species 111-114 mitogen-activated protein kinase 8 Rattus norvegicus 134-137 21134288-9 2010 ROS production leads to activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun-N-terminal kinase (JNK) and then activation of the NF-kappaB transcription factor. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Rattus norvegicus 93-116 21134288-9 2010 ROS production leads to activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun-N-terminal kinase (JNK) and then activation of the NF-kappaB transcription factor. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Rattus norvegicus 118-121 21134288-12 2010 CONCLUSIONS: Collectively, in RBA-1 cells, activation of ERK1/2- and JNK-NF-kappaB cascades by a ROS-dependent manner is essential for MMP-9 up-regulation/activation and cell migration induced by TGF-beta1. Reactive Oxygen Species 97-100 mitogen-activated protein kinase 8 Rattus norvegicus 69-72 20863874-8 2010 It is suggested from our results that reactive oxygen species (ROS) have a mediation effect to oxidative stress and up-regulation of JNK and P53 phosphorylation involved in mechanistic pathways of TiO(2)-NPs can induce apoptosis and cell cycle arrest in PC12 cells. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 8 Rattus norvegicus 133-136 19332540-8 2009 Thus, mitochondria-derived ROS induced by palmitate may be major contributors to JNK activation and cellular insulin resistance. Reactive Oxygen Species 27-30 mitogen-activated protein kinase 8 Rattus norvegicus 81-84 19332540-5 2009 Among the well established stimuli for JNK activation, reactive oxygen species (ROS) played a causal role in palmitate-induced JNK activation. Reactive Oxygen Species 55-78 mitogen-activated protein kinase 8 Rattus norvegicus 39-42 19332540-5 2009 Among the well established stimuli for JNK activation, reactive oxygen species (ROS) played a causal role in palmitate-induced JNK activation. Reactive Oxygen Species 55-78 mitogen-activated protein kinase 8 Rattus norvegicus 127-130 19332540-5 2009 Among the well established stimuli for JNK activation, reactive oxygen species (ROS) played a causal role in palmitate-induced JNK activation. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 8 Rattus norvegicus 39-42 19332540-5 2009 Among the well established stimuli for JNK activation, reactive oxygen species (ROS) played a causal role in palmitate-induced JNK activation. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 8 Rattus norvegicus 127-130 20686488-0 2010 Glomerular angiotensinogen is induced in mesangial cells in diabetic rats via reactive oxygen species--ERK/JNK pathways. Reactive Oxygen Species 78-101 mitogen-activated protein kinase 8 Rattus norvegicus 107-110 20828747-9 2010 The observed decrease in GSH/GSSG ratio and activation of JNK in the reperfused heart suggested that proteolysis could be triggered by reactive oxygen species. Reactive Oxygen Species 135-158 mitogen-activated protein kinase 8 Rattus norvegicus 58-61 17359975-11 2007 AGEs-induced ROS subsequently activates MAPK (p38, JNK and ERK1/2) and NF-kB. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Rattus norvegicus 51-54 18178252-2 2008 Complement induces production of reactive oxygen species (ROS) via the NAPDH oxidase, and stimulates phosphorylation of c-Jun N-terminal kinase (JNK) and p38 kinase in a ROS-dependent manner. Reactive Oxygen Species 170-173 mitogen-activated protein kinase 8 Rattus norvegicus 120-143 18178252-2 2008 Complement induces production of reactive oxygen species (ROS) via the NAPDH oxidase, and stimulates phosphorylation of c-Jun N-terminal kinase (JNK) and p38 kinase in a ROS-dependent manner. Reactive Oxygen Species 170-173 mitogen-activated protein kinase 8 Rattus norvegicus 145-148 17869266-6 2008 Pretreatment with a catalase/superoxide dismutase mimetic or adenoviral-mediated expression of catalase or a dominant-negative c-jun N-terminal kinase-1 (JNK) mutant inhibited the betaAR- and H(2)O(2)-stimulated increases in EMMPRIN expression suggesting that EMMPRIN expression is regulated via a reactive oxygen species-dependent JNK pathway. Reactive Oxygen Species 298-321 mitogen-activated protein kinase 8 Rattus norvegicus 127-152 17869266-6 2008 Pretreatment with a catalase/superoxide dismutase mimetic or adenoviral-mediated expression of catalase or a dominant-negative c-jun N-terminal kinase-1 (JNK) mutant inhibited the betaAR- and H(2)O(2)-stimulated increases in EMMPRIN expression suggesting that EMMPRIN expression is regulated via a reactive oxygen species-dependent JNK pathway. Reactive Oxygen Species 298-321 mitogen-activated protein kinase 8 Rattus norvegicus 154-157 17869266-9 2008 Thus, in cardiac myocytes betaAR stimulation induces the expression of EMMPRIN via the ROS-dependent activation of JNK. Reactive Oxygen Species 87-90 mitogen-activated protein kinase 8 Rattus norvegicus 115-118 17258167-4 2007 The NADPH oxidase-derived ROS signal then allows via Yes, JNK, and EGFR activation for CD95 tyrosine phosphorylation as a prerequisite for CD95 targeting to the plasma membrane and formation of the death inducing signalling complex. Reactive Oxygen Species 26-29 mitogen-activated protein kinase 8 Rattus norvegicus 58-61 17533154-7 2007 A Galpha(12/13)-inhibitory polypeptide derived from the regulator of the G-protein signaling domain of p115-Rho guanine nucleotide exchange factor and a JNK inhibitor, SP600125, suppressed the ET-1-induced increase in expression of marker proteins of myofibroblast formation through a Galpha(12/13)-reactive oxygen species-JNK pathway. Reactive Oxygen Species 299-322 mitogen-activated protein kinase 8 Rattus norvegicus 153-156 17533154-7 2007 A Galpha(12/13)-inhibitory polypeptide derived from the regulator of the G-protein signaling domain of p115-Rho guanine nucleotide exchange factor and a JNK inhibitor, SP600125, suppressed the ET-1-induced increase in expression of marker proteins of myofibroblast formation through a Galpha(12/13)-reactive oxygen species-JNK pathway. Reactive Oxygen Species 299-322 mitogen-activated protein kinase 8 Rattus norvegicus 323-326 17438009-3 2007 Cisplatin promotes increased production of reactive oxygen species, which can activate c-jun N-terminal kinase (JNK) that is a mediator of apoptosis and can lead to increased expression of proinflammatory mediators that could intensify the cytotoxic effects of cisplatin. Reactive Oxygen Species 43-66 mitogen-activated protein kinase 8 Rattus norvegicus 87-110 17438009-3 2007 Cisplatin promotes increased production of reactive oxygen species, which can activate c-jun N-terminal kinase (JNK) that is a mediator of apoptosis and can lead to increased expression of proinflammatory mediators that could intensify the cytotoxic effects of cisplatin. Reactive Oxygen Species 43-66 mitogen-activated protein kinase 8 Rattus norvegicus 112-115 17038326-15 2006 These results show that opening of mitochondrial K(ATP) channels and generation of reactive oxygen species, in association with phosphorylation of Akt, ERK, and JNK, and increased expression of NOS and Bcl-2, play an essential role in the protective effect of PKGIalpha. Reactive Oxygen Species 83-106 mitogen-activated protein kinase 8 Rattus norvegicus 161-164 16174550-10 2006 The findings suggest that Akt1 regulating JNK scaffold and then regulating JNK activation were closely associated with reactive oxygen species (ROS) during cerebral ischemia. Reactive Oxygen Species 119-142 mitogen-activated protein kinase 8 Rattus norvegicus 42-45 17210797-0 2007 Mitochondrial c-Jun NH2-terminal kinase prevents the accumulation of reactive oxygen species and reduces necrotic damage in neural tumor cells that lack trophic support. Reactive Oxygen Species 69-92 mitogen-activated protein kinase 8 Rattus norvegicus 14-39 17210797-5 2007 Pharmacologic inhibition of JNK provoked a further increase of the DeltaPsi(M), an increase in reactive oxygen species (ROS) production, and a sustained decrease in cell viability due to necrosis. Reactive Oxygen Species 95-118 mitogen-activated protein kinase 8 Rattus norvegicus 28-31 17210797-5 2007 Pharmacologic inhibition of JNK provoked a further increase of the DeltaPsi(M), an increase in reactive oxygen species (ROS) production, and a sustained decrease in cell viability due to necrosis. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Rattus norvegicus 28-31 17210797-9 2007 These data indicate that local activation of JNK in the mitochondria can protect against necrotic cell death associated with ROS production, facilitating the growth of neural tumor cells subjected to serum deprivation. Reactive Oxygen Species 125-128 mitogen-activated protein kinase 8 Rattus norvegicus 45-48 17041759-0 2006 Norepinephrine induces apoptosis in neonatal rat endothelial cells via a ROS-dependent JNK activation pathway. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Rattus norvegicus 87-90 17041759-13 2006 In conclusions, our study is the first report documenting that NE induces apoptosis in neonatal rat endothelial cells via a ROS-dependent JNK activation pathway. Reactive Oxygen Species 124-127 mitogen-activated protein kinase 8 Rattus norvegicus 138-141 16174550-10 2006 The findings suggest that Akt1 regulating JNK scaffold and then regulating JNK activation were closely associated with reactive oxygen species (ROS) during cerebral ischemia. Reactive Oxygen Species 119-142 mitogen-activated protein kinase 8 Rattus norvegicus 75-78 16174550-10 2006 The findings suggest that Akt1 regulating JNK scaffold and then regulating JNK activation were closely associated with reactive oxygen species (ROS) during cerebral ischemia. Reactive Oxygen Species 144-147 mitogen-activated protein kinase 8 Rattus norvegicus 42-45 16174550-10 2006 The findings suggest that Akt1 regulating JNK scaffold and then regulating JNK activation were closely associated with reactive oxygen species (ROS) during cerebral ischemia. Reactive Oxygen Species 144-147 mitogen-activated protein kinase 8 Rattus norvegicus 75-78 16143311-9 2005 Our observations imply that genipin signaling to apoptosis of hepatoma cells is mediated via NADPH oxidase-dependent generation of ROS, which leads to downstream of JNK. Reactive Oxygen Species 131-134 mitogen-activated protein kinase 8 Rattus norvegicus 165-168 15917250-8 2005 Only Yes and JNK activation were sensitive to N-acetylcysteine, inhibitors of NADPH oxidase, PKCzeta, or sphingomyelinase, indicating that the CD95L-induced ROS response is upstream of Yes and JNK but not of Fyn and c-Src activation. Reactive Oxygen Species 157-160 mitogen-activated protein kinase 8 Rattus norvegicus 193-196 15936777-6 2005 Moreover, G activated JNK; JNK activation was reduced by co-incubation with the calcium channel blocker verapamil and with the ROS scavengers superoxide dismutase and catalase. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Rattus norvegicus 27-30 12574140-0 2003 Beta-adrenergic receptor-stimulated apoptosis in cardiac myocytes is mediated by reactive oxygen species/c-Jun NH2-terminal kinase-dependent activation of the mitochondrial pathway. Reactive Oxygen Species 81-104 mitogen-activated protein kinase 8 Rattus norvegicus 105-130 15743761-2 2005 Among three MAPKs, c-Jun NH(2)-terminal kinase (JNK) and p38 MAPK required ROS production for activation, as an NADPH oxidase inhibitor, diphenyleneiodonium, inhibited the activation. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 8 Rattus norvegicus 19-46 15743761-2 2005 Among three MAPKs, c-Jun NH(2)-terminal kinase (JNK) and p38 MAPK required ROS production for activation, as an NADPH oxidase inhibitor, diphenyleneiodonium, inhibited the activation. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 8 Rattus norvegicus 48-51 15743761-11 2005 These results suggest that Galpha(12/13)-mediated ROS production through Rho and Rac is essential for JNK and p38 MAPK activation. Reactive Oxygen Species 50-53 mitogen-activated protein kinase 8 Rattus norvegicus 102-105 15824196-10 2005 These results suggest that the preconditioning effects of Ang II for cardiac I/R injury may be mediated by cardiac mitochondria-derived ROS enhanced through NAD(P)H oxidase via JNK and p38 mitogen-activated protein kinase activation. Reactive Oxygen Species 136-139 mitogen-activated protein kinase 8 Rattus norvegicus 177-180 11912218-3 2002 The evidence is consistent with the view that irradiation induced an increase in reactive oxygen species and that this leads to stimulation of the stress-activated protein kinase, JNK, and activation of the transcription factor, c-Jun. Reactive Oxygen Species 81-104 mitogen-activated protein kinase 8 Rattus norvegicus 180-183 12193730-10 2002 AA may activate the NADPH oxidase, leading to production of reactive oxygen species, which in turn mediate the activation of JNK. Reactive Oxygen Species 60-83 mitogen-activated protein kinase 8 Rattus norvegicus 125-128