PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33930940-5 2021 Moreover, the activities of antioxidant enzymes were greatly up-regulated by AgNPs, which eventually inhibited the generation of reactive oxygen species (ROS) induced by As(III) and the downstream stress-activated protein kinases/c-Jun amino-terminal kinases (SAPK/JNK) signaling pathway. Reactive Oxygen Species 154-157 mitogen-activated protein kinase 8 Homo sapiens 265-268 34054302-15 2021 Salusin-beta exacerbated inflammation and apoptosis, upregulated intracellular ROS production in HG-induced HRECs, and activated ROS-dependent JNK and p38 MAPK signalling, while knockdown of salusin-beta suppressed these effects. Reactive Oxygen Species 129-132 mitogen-activated protein kinase 8 Homo sapiens 143-146 33895649-11 2021 These results showed that 3-DSC-related G2/M phase cell cycle arrest and apoptosis by JNK/p38 MAPK signaling pathway in ESCC cells were mediated by ROS. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Homo sapiens 86-89 33895649-12 2021 CONCLUSION: ROS generation by 3-DSC in cancer cells could be an attractive strategy for apoptosis of cancer cells by inducing cell cycle arrest, ER stress, MMP loss, multi-caspase activity, and JNK/p38 MAPK pathway. Reactive Oxygen Species 12-15 mitogen-activated protein kinase 8 Homo sapiens 194-197 34054302-16 2021 Conclusion: Our findings indicate that salusin-beta can promote inflammation and apoptosis via ROS-dependent JNK and p38 MAPK signalling in HG-induced HRECs and could be a therapeutic target for DR. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 8 Homo sapiens 109-112 33791802-6 2021 Mechanistically, PLB induced apoptosis and autophagy by generating reactive oxygen species to mediate JNK and AKT/mTOR pathways. Reactive Oxygen Species 67-90 mitogen-activated protein kinase 8 Homo sapiens 102-105 33959604-7 2021 Mechanistically, the combined treatment resulted in an excessive accumulation of intracellular reactive oxygen species (ROS), which leads to the activation of endoplasmic reticulum (ER) stress and the JNK signaling pathway in human prostate cancer cells. Reactive Oxygen Species 95-118 mitogen-activated protein kinase 8 Homo sapiens 201-204 33959604-7 2021 Mechanistically, the combined treatment resulted in an excessive accumulation of intracellular reactive oxygen species (ROS), which leads to the activation of endoplasmic reticulum (ER) stress and the JNK signaling pathway in human prostate cancer cells. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 201-204 33159186-4 2021 Here we propose that this increased ROS production not only causes oxidative damage but also ultimately induces an oxidative stress response that reactivates the redox-sensitive AMPK and activates the redox-sensitive stress kinase JNK. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 231-234 33871094-3 2021 LPS and Gram-Negative bacteria induce reactive oxygen species (ROS) -dependent NETs formation via JNK pathway. Reactive Oxygen Species 38-61 mitogen-activated protein kinase 8 Homo sapiens 98-101 33871094-3 2021 LPS and Gram-Negative bacteria induce reactive oxygen species (ROS) -dependent NETs formation via JNK pathway. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 8 Homo sapiens 98-101 33871094-8 2021 Additional data indicate that these effects are mediated by suppressing ROS production at least partly via inhibiting JNK activation and depleting NAD(P)H. Reactive Oxygen Species 72-75 mitogen-activated protein kinase 8 Homo sapiens 118-121 33674562-7 2021 In combination with BTZ, CPX promotes apoptosis in GBM cells through the induction of reactive oxygen species (ROS)-mediated c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling. Reactive Oxygen Species 86-109 mitogen-activated protein kinase 8 Homo sapiens 125-148 33674562-7 2021 In combination with BTZ, CPX promotes apoptosis in GBM cells through the induction of reactive oxygen species (ROS)-mediated c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling. Reactive Oxygen Species 86-109 mitogen-activated protein kinase 8 Homo sapiens 150-153 33674562-7 2021 In combination with BTZ, CPX promotes apoptosis in GBM cells through the induction of reactive oxygen species (ROS)-mediated c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling. Reactive Oxygen Species 111-114 mitogen-activated protein kinase 8 Homo sapiens 125-148 33674562-7 2021 In combination with BTZ, CPX promotes apoptosis in GBM cells through the induction of reactive oxygen species (ROS)-mediated c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling. Reactive Oxygen Species 111-114 mitogen-activated protein kinase 8 Homo sapiens 150-153 32335916-8 2020 Then, the active Mst1-JNK pathway mediated mitochondrial reactive oxygen species (mROS) overproduction and then excessive ROS induced cancer cell death. Reactive Oxygen Species 57-80 mitogen-activated protein kinase 8 Homo sapiens 22-25 33045079-11 2021 Treatment of irradiated cells with SP600125, a JNK inhibitor, augmented ROS production and impeded cell migration. Reactive Oxygen Species 72-75 mitogen-activated protein kinase 8 Homo sapiens 47-50 33613824-0 2021 Coronary Endothelium No-Reflow Injury Is Associated with ROS-Modified Mitochondrial Fission through the JNK-Drp1 Signaling Pathway. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 8 Homo sapiens 104-107 33613824-7 2021 Our results also demonstrated that ROS stimulated mitochondrial fission via JNK-mediated Drp1 phosphorylation. Reactive Oxygen Species 35-38 mitogen-activated protein kinase 8 Homo sapiens 76-79 33613824-8 2021 These findings indicate that the ROS-JNK-Drp1 signaling pathway may be one of the molecular mechanisms underlying endothelial cell damage during H/R injury. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 37-40 33532038-10 2021 Further studies demonstrated that emodin induces necroptosis through ROS-mediated activation of JNK signaling pathway and also inhibits glycolysis by downregulation of GLUT1 through ROS-mediated inactivation of the PI3K/AKT signaling pathway. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 8 Homo sapiens 96-99 33502699-0 2021 Synergistic anticancer effect of docosahexaenoic acid and isoliquiritigenin on human colorectal cancer cells through ROS-mediated regulation of the JNK and cytochrome c release. Reactive Oxygen Species 117-120 mitogen-activated protein kinase 8 Homo sapiens 148-151 33502699-8 2021 Our data also demonstrated that cotreating with DHA and ISL strongly upregulated the phosphorylation of ERK and JNK, which are functionally associated with ROS induced by the two compounds in combination. Reactive Oxygen Species 156-159 mitogen-activated protein kinase 8 Homo sapiens 112-115 33502699-10 2021 Excessive ROS-induced JNK activation and cytochrome c release from mitochondria played a key role in the synergistic anticancer activity of CRC cells by cotreating with DHA and ISL. Reactive Oxygen Species 10-13 mitogen-activated protein kinase 8 Homo sapiens 22-25 33039870-0 2021 Bisphenol A induces apoptosis through GPER-dependent activation of the ROS/Ca2+-ASK1-JNK pathway in human granulosa cell line KGN. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Homo sapiens 85-88 33039870-10 2021 These results suggest that BPA exposure induces KGN cell apoptosis through GPER-dependent activation of the ROS/Ca2+-ASK1-JNK signaling pathway. Reactive Oxygen Species 108-111 mitogen-activated protein kinase 8 Homo sapiens 122-125 32335916-8 2020 Then, the active Mst1-JNK pathway mediated mitochondrial reactive oxygen species (mROS) overproduction and then excessive ROS induced cancer cell death. Reactive Oxygen Species 83-86 mitogen-activated protein kinase 8 Homo sapiens 22-25 33299528-7 2020 With reduced NRF2 SUMOylation, increased ROS acted as signaling molecules to activate the JNK/c-Jun axis, which enhanced cell mobility and cell adhesion, to promote LUAD cell migration and invasion. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 8 Homo sapiens 90-93 32787872-13 2020 Ethanol-induced JNK1 phosphorylation activated the NLRP3 inflammasome that induced caspase-1 dependent mitophagy inhibition, thereby exacerbating ROS accumulation and causing cell death. Reactive Oxygen Species 146-149 mitogen-activated protein kinase 8 Homo sapiens 16-20 33116501-12 2020 Conclusion: Our results suggested that the combination of AgNTs and GEM possessed broad-spectrum and potent synergistic anti-glioma activity, resulting from cell apoptosis mediated by a ROS-dependent mitochondrial pathway in which JNK might be involved. Reactive Oxygen Species 186-189 mitogen-activated protein kinase 8 Homo sapiens 231-234 33072762-0 2020 Isodeoxyelephantopin Inactivates Thioredoxin Reductase 1 and Activates ROS-Mediated JNK Signaling Pathway to Exacerbate Cisplatin Effectiveness in Human Colon Cancer Cells. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Homo sapiens 84-87 33072762-6 2020 Furthermore, our results showed that ESI treatment markedly increased cellular reactive oxygen species (ROS) levels by inhibiting thioredoxin reductase 1 (TrxR1) activity, which leads to activation of the JNK signaling pathway and eventually cell death in HCT116 and RKO cells. Reactive Oxygen Species 104-107 mitogen-activated protein kinase 8 Homo sapiens 205-208 33072762-8 2020 Combination of ESI and cisplatin significantly increased the production of ROS, resulting in activation of the JNK signaling pathway in HCT116 and RKO cells. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 8 Homo sapiens 111-114 33130826-0 2020 Photodynamic therapy induces autophagy-mediated cell death in human colorectal cancer cells via activation of the ROS/JNK signaling pathway. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Homo sapiens 118-121 33130826-10 2020 In conclusion, inhibition of autophagy can remarkably alleviate PDT-mediated anticancer efficiency in CRC cells via inactivation of the ROS/JNK signaling pathway. Reactive Oxygen Species 136-139 mitogen-activated protein kinase 8 Homo sapiens 140-143 33133132-3 2020 We found that knockdown of Setdb1 impaired cell proliferation, led to an increase in reactive oxygen species (ROS) level through NADPH oxidase, and Setdb1 deficiency activated ROS downstream signaling pathways, including JNK and p38 MAPK, which possibly contributed to SSC apoptosis. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 8 Homo sapiens 221-224 33133132-3 2020 We found that knockdown of Setdb1 impaired cell proliferation, led to an increase in reactive oxygen species (ROS) level through NADPH oxidase, and Setdb1 deficiency activated ROS downstream signaling pathways, including JNK and p38 MAPK, which possibly contributed to SSC apoptosis. Reactive Oxygen Species 176-179 mitogen-activated protein kinase 8 Homo sapiens 221-224 32715490-10 2020 CONCLUSIONS: Citbismine-E is a powerful cytotoxic agent against HL-60 cells that acts by inducing mitochondrial dysfunction-mediated apoptosis through ROS-dependent JNK activation. Reactive Oxygen Species 151-154 mitogen-activated protein kinase 8 Homo sapiens 165-168 32782585-10 2020 The synthetic lethal interaction between ROS accumulation and Ras effector JNK activation may be critical for enhancing the sensitivity to ferroptotic cell death mediated by xCT inhibitor, SAS. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 8 Homo sapiens 75-78 32752099-0 2020 Induction of Apoptosis by Coptisine in Hep3B Hepatocellular Carcinoma Cells through Activation of the ROS-Mediated JNK Signaling Pathway. Reactive Oxygen Species 102-105 mitogen-activated protein kinase 8 Homo sapiens 115-118 32922532-6 2020 In addition, reactive oxygen species (ROS) increased dramatically after Propranolol treatment and Propranolol activated the phosphorylation of JNK. Reactive Oxygen Species 13-36 mitogen-activated protein kinase 8 Homo sapiens 143-146 32922532-6 2020 In addition, reactive oxygen species (ROS) increased dramatically after Propranolol treatment and Propranolol activated the phosphorylation of JNK. Reactive Oxygen Species 38-41 mitogen-activated protein kinase 8 Homo sapiens 143-146 32922532-9 2020 In summary, these results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 8 Homo sapiens 117-120 32752099-9 2020 It is worth noting that coptisine significantly upregulated phosphorylation of ROS-dependent c-Jun N-terminal kinase (JNK), whereas treatment with JNK inhibitor could suppress an apoptosis-related series event. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 93-116 32752099-9 2020 It is worth noting that coptisine significantly upregulated phosphorylation of ROS-dependent c-Jun N-terminal kinase (JNK), whereas treatment with JNK inhibitor could suppress an apoptosis-related series event. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 118-121 32752099-10 2020 Taken together, our results suggest that coptisine has an anticancer effect in Hep3B cells through ROS-mediated activation of the JNK signaling pathway. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 8 Homo sapiens 130-133 32294550-11 2020 ROS might contribute to ER stress and further induce apoptosis via the JNK/p53/p21 pathway. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 71-74 32629820-0 2020 Picropodophyllotoxin, an Epimer of Podophyllotoxin, Causes Apoptosis of Human Esophageal Squamous Cell Carcinoma Cells Through ROS-Mediated JNK/P38 MAPK Pathways. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 140-143 32551381-6 2020 We propose the sustained low-level activation of JNK and the inhibition of NF-kappaB promoted ROS (Reactive Oxygen Species) production that yielded the observed cell death. Reactive Oxygen Species 94-97 mitogen-activated protein kinase 8 Homo sapiens 49-52 32551381-6 2020 We propose the sustained low-level activation of JNK and the inhibition of NF-kappaB promoted ROS (Reactive Oxygen Species) production that yielded the observed cell death. Reactive Oxygen Species 99-122 mitogen-activated protein kinase 8 Homo sapiens 49-52 32236589-7 2020 Additionally, JNK activation and cell cycle arrest at the G2/M phase were prevented by administration of an ROS scavenger. Reactive Oxygen Species 108-111 mitogen-activated protein kinase 8 Homo sapiens 14-17 32236589-9 2020 Together, the results of the present study suggest that andrographolide caused G2/M arrest and induced cell apoptosis via regulation of the ROS/JNK signaling pathway in osteosarcoma cells. Reactive Oxygen Species 140-143 mitogen-activated protein kinase 8 Homo sapiens 144-147 32236589-0 2020 Andrographolide induces apoptosis in human osteosarcoma cells via the ROS/JNK pathway. Reactive Oxygen Species 70-73 mitogen-activated protein kinase 8 Homo sapiens 74-77 32429320-1 2020 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species 16-39 mitogen-activated protein kinase 8 Homo sapiens 58-85 32523687-5 2020 Here, we show that activation of p38 and JNK partially contributed to sustained adenosine-induced mitochondrial reactive oxygen species production. Reactive Oxygen Species 112-135 mitogen-activated protein kinase 8 Homo sapiens 41-44 32429320-1 2020 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species 16-39 mitogen-activated protein kinase 8 Homo sapiens 87-93 32429320-1 2020 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 8 Homo sapiens 58-85 32429320-1 2020 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 8 Homo sapiens 87-93 32429320-2 2020 JNK1/2 are not only regulated by ROS-they in turn can also control ROS production. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 0-6 32429320-2 2020 JNK1/2 are not only regulated by ROS-they in turn can also control ROS production. Reactive Oxygen Species 67-70 mitogen-activated protein kinase 8 Homo sapiens 0-6 32429320-4 2020 Here, we provide evidence that establishes p66Shc, an oxidoreductase, as a JNK1/2 effector downstream of Rigosertib-induced ROS production, DNA damage, and cell death. Reactive Oxygen Species 124-127 mitogen-activated protein kinase 8 Homo sapiens 75-81 32131874-10 2020 ROS, MMP-3 expression, and IL-6 was suppressed by administering 30 muM of SP600125 (a JNK inhibitor) in MH7A cells. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 86-89 32308415-0 2020 Irinotecan Induces Autophagy-Dependent Apoptosis and Positively Regulates ROS-Related JNK- and P38-MAPK Pathways in Gastric Cancer Cells. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 86-89 32308415-11 2020 Conclusion: Taken together, these results indicate that IRI stimulates the ROS-related JNK- and p38-MAPK pathways to promote autophagy-dependent apoptosis. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 8 Homo sapiens 87-90 32308804-7 2020 In addition, the combination treatment of PLB and cisplatin resulted in a synergistic inhibition of TSCC viability, apoptosis, and autophagy by increasing intracellular ROS, which may be achieved by activating JNK and inhibiting AKT/mTOR signaling pathways. Reactive Oxygen Species 169-172 mitogen-activated protein kinase 8 Homo sapiens 210-213 32106366-0 2020 Magnoflorine inhibits human gastric cancer progression by inducing autophagy, apoptosis and cell cycle arrest by JNK activation regulated by ROS. Reactive Oxygen Species 141-144 mitogen-activated protein kinase 8 Homo sapiens 113-116 32260423-5 2020 Moreover, compound 8a effectively killed tumor cells by reactive oxygen species (ROS)-JNK activation, causing an increase in ROS levels, JNK phosphorylation, and mitochondrial stress. Reactive Oxygen Species 56-79 mitogen-activated protein kinase 8 Homo sapiens 86-89 32260423-5 2020 Moreover, compound 8a effectively killed tumor cells by reactive oxygen species (ROS)-JNK activation, causing an increase in ROS levels, JNK phosphorylation, and mitochondrial stress. Reactive Oxygen Species 81-84 mitogen-activated protein kinase 8 Homo sapiens 86-89 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 8 Homo sapiens 126-129 31707583-7 2020 LCH also induced apoptosis of ESCC cells through reactive oxygen species-mediated endoplasmic reticulum (ER) stress via JNK/p38 activation pathways. Reactive Oxygen Species 49-72 mitogen-activated protein kinase 8 Homo sapiens 120-123 32521858-0 2020 Taraxastane inhibits the proliferation, migration and invasion of human cervical cancer by inducing ROS- mediated necrosis like cell death, cell cycle arrest and modulation of JNK/MAPK signaling pathway. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 8 Homo sapiens 176-179 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 8 Homo sapiens 120-123 31506575-7 2019 Moreover, downregulation of JNK by its specific inhibitor SP600125 significantly diminished the anticancer activity of APE indicating that ROS generation and sustained JNK activation represented the main underlying mechanism of APE-induced cell death. Reactive Oxygen Species 139-142 mitogen-activated protein kinase 8 Homo sapiens 28-31 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 8 Homo sapiens 29-32 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Reactive Oxygen Species 66-89 mitogen-activated protein kinase 8 Homo sapiens 119-142 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Reactive Oxygen Species 66-89 mitogen-activated protein kinase 8 Homo sapiens 144-147 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Reactive Oxygen Species 66-89 mitogen-activated protein kinase 8 Homo sapiens 268-271 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 8 Homo sapiens 119-142 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 8 Homo sapiens 144-147 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 8 Homo sapiens 268-271 31212128-3 2019 This leads to elevated phosphorylated-c-Jun N-terminal kinase (p-JNK), which further activates reactive oxygen species (ROS), initiates an inflammatory response, and finally leads to severe hepatic injury. Reactive Oxygen Species 95-118 mitogen-activated protein kinase 8 Homo sapiens 65-68 31212128-3 2019 This leads to elevated phosphorylated-c-Jun N-terminal kinase (p-JNK), which further activates reactive oxygen species (ROS), initiates an inflammatory response, and finally leads to severe hepatic injury. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 65-68 31396402-7 2019 Enhanced ROS generation by pristimerin activated the ASK1/JNK signaling pathway. Reactive Oxygen Species 9-12 mitogen-activated protein kinase 8 Homo sapiens 58-61 31547311-0 2019 Anti-Metabolic Syndrome Effects of Fucoidan from Fucus vesiculosus via Reactive Oxygen Species-Mediated Regulation of JNK, Akt, and AMPK Signaling. Reactive Oxygen Species 71-94 mitogen-activated protein kinase 8 Homo sapiens 118-121 31547311-6 2019 Thus, FvF increased glucose consumption and relieved IR via ROS-mediated JNK and Akt signaling pathways. Reactive Oxygen Species 60-63 mitogen-activated protein kinase 8 Homo sapiens 73-76 31176737-6 2019 Our results show that WZ26 targets thioredoxin reductase 1 (TrxR1) and increases cellular reactive oxygen species (ROS) levels, which results in the activation of JNK signaling pathway in human colon cancer cells. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 8 Homo sapiens 163-166 31357564-9 2019 Collectively, these data demonstrated that erianin inhibited proliferation and induced apoptosis of HaCaT cells through ROS-mediated JNK/c-Jun and AKT/mTOR signaling pathways. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 133-136 31336784-5 2019 We discovered that ROS was accumulated in NMP-treated NSCLC cells, followed by c-Jun N-terminal kinase (JNK) and p38 MAP kinase (p38) activation. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 8 Homo sapiens 79-102 31336784-5 2019 We discovered that ROS was accumulated in NMP-treated NSCLC cells, followed by c-Jun N-terminal kinase (JNK) and p38 MAP kinase (p38) activation. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 8 Homo sapiens 104-107 31360110-9 2019 Pretreatment of cells with the ROS reversal agent NAC significantly blocked the apoptosis induced by the combination treatment, and suppressed expression of JNK and p38 phosphorylation in HCT116 and RKO cells. Reactive Oxygen Species 31-34 mitogen-activated protein kinase 8 Homo sapiens 157-160 31118030-8 2019 Using cytosolic ROS antioxidant NAC, we found that p38 and JNK are downstream signals of ROS and involve in NaIO3-induced cytotoxicity but not in mitochondrial dynamics, while ROS is also involved in LC3II expression. Reactive Oxygen Species 16-19 mitogen-activated protein kinase 8 Homo sapiens 59-62 31118030-8 2019 Using cytosolic ROS antioxidant NAC, we found that p38 and JNK are downstream signals of ROS and involve in NaIO3-induced cytotoxicity but not in mitochondrial dynamics, while ROS is also involved in LC3II expression. Reactive Oxygen Species 89-92 mitogen-activated protein kinase 8 Homo sapiens 59-62 31118030-8 2019 Using cytosolic ROS antioxidant NAC, we found that p38 and JNK are downstream signals of ROS and involve in NaIO3-induced cytotoxicity but not in mitochondrial dynamics, while ROS is also involved in LC3II expression. Reactive Oxygen Species 89-92 mitogen-activated protein kinase 8 Homo sapiens 59-62 31551215-5 2019 Furthermore, reactive oxygen species (ROS) stimulated the phosphorylation of ERK, p38 and JNK, while pre-administration of quercetin significantly (P<0.05) reduced the phosphorylation. Reactive Oxygen Species 38-41 mitogen-activated protein kinase 8 Homo sapiens 90-93 31139404-8 2019 These collective data indicate that HTE induces apoptosis via ROS production through the p38, JNK, and caspase-3-dependent pathways. Reactive Oxygen Species 62-65 mitogen-activated protein kinase 8 Homo sapiens 94-97 30810066-4 2019 In vitro analyses revealed that ROS production was induced by recombinant and adenoviral vector-mediated IGFBP-5 (AdBP5) in a dose- and time-dependent manner, regulated through MEK/ERK and JNK signaling, and primarily mediated by NADPH oxidase (Nox). Reactive Oxygen Species 32-35 mitogen-activated protein kinase 8 Homo sapiens 189-192 29511793-0 2019 Calcifying nanoparticles induce cytotoxicity mediated by ROS-JNK signaling pathways. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 8 Homo sapiens 61-64 31019655-0 2019 Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway. Reactive Oxygen Species 97-100 mitogen-activated protein kinase 8 Homo sapiens 110-113 31019655-8 2019 ROS scavenger NAC rescued SNX-2112/TRAIL-induced apoptosis and suppressed SNX-2112-induced p-JNK and p53. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 93-96 30850584-7 2019 These data revealed a previously unknown mechanism that BNIP3-induced autophagy occurs through hypoxia-induced ROS-mediated p38 and JNK MAPK activation and supports the migration of epidermal keratinocytes during wound healing. Reactive Oxygen Species 111-114 mitogen-activated protein kinase 8 Homo sapiens 132-135 31229492-8 2019 ROS produced by iron activates various signalling pathways, including mitogen-activated protein kinase (MAPK) signalling pathways such as the apoptosis signal-regulating kinase 1 (ASK1)-p38/JNK pathway. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 190-193 31387985-5 2019 By RNA interference and ectopic Hic-5 expression, we demonstrated Hic-5 was essential for activation of NADPH oxidase and ROS generation leading to activation of downstream JNK and c-jun transcription factor. Reactive Oxygen Species 122-125 mitogen-activated protein kinase 8 Homo sapiens 173-176 31387985-8 2019 Thus Hic-5 was both downstream and upstream of NADPH oxidase-ROS-JNK-c-jun cascade. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 8 Homo sapiens 65-68 31290253-7 2019 Further studies revealed that pristimerin could produce excessive reactive oxygen species (ROS), which then induce JNK activation. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 8 Homo sapiens 115-118 31357564-0 2019 Erianin Inhibits Proliferation and Induces Apoptosis of HaCaT Cells via ROS-Mediated JNK/c-Jun and AKT/mTOR Signaling Pathways. Reactive Oxygen Species 72-75 mitogen-activated protein kinase 8 Homo sapiens 85-88 31233063-0 2019 A surface-layer protein from Lactobacillus acidophilus NCFM induces autophagic death in HCT116 cells requiring ROS-mediated modulation of mTOR and JNK signaling pathways. Reactive Oxygen Species 111-114 mitogen-activated protein kinase 8 Homo sapiens 147-150 30556404-7 2019 A positive feedback loop between calcium (Ca2+) and c-Jun N-terminal kinase (JNK) occurred following ROS generation, leading to lysosomal membrane permeabilization and mitochondrial dysfunction. Reactive Oxygen Species 101-104 mitogen-activated protein kinase 8 Homo sapiens 52-75 30556404-7 2019 A positive feedback loop between calcium (Ca2+) and c-Jun N-terminal kinase (JNK) occurred following ROS generation, leading to lysosomal membrane permeabilization and mitochondrial dysfunction. Reactive Oxygen Species 101-104 mitogen-activated protein kinase 8 Homo sapiens 77-80 31101341-7 2019 Furthermore, Iso was functioned as reactive oxygen species (ROS) scavenger that markedly hindered c-Jun N-terminal kinases (JNK) signaling activation in UVB-treated HFDs. Reactive Oxygen Species 35-58 mitogen-activated protein kinase 8 Homo sapiens 98-122 31101341-7 2019 Furthermore, Iso was functioned as reactive oxygen species (ROS) scavenger that markedly hindered c-Jun N-terminal kinases (JNK) signaling activation in UVB-treated HFDs. Reactive Oxygen Species 35-58 mitogen-activated protein kinase 8 Homo sapiens 124-127 31101341-7 2019 Furthermore, Iso was functioned as reactive oxygen species (ROS) scavenger that markedly hindered c-Jun N-terminal kinases (JNK) signaling activation in UVB-treated HFDs. Reactive Oxygen Species 60-63 mitogen-activated protein kinase 8 Homo sapiens 98-122 31101341-7 2019 Furthermore, Iso was functioned as reactive oxygen species (ROS) scavenger that markedly hindered c-Jun N-terminal kinases (JNK) signaling activation in UVB-treated HFDs. Reactive Oxygen Species 60-63 mitogen-activated protein kinase 8 Homo sapiens 124-127 30904015-8 2019 Moreover, the results showed an increase in ROS production linked with JNK activation following the enhancement of dehydrogenase activity. Reactive Oxygen Species 44-47 mitogen-activated protein kinase 8 Homo sapiens 71-74 30981511-8 2019 Interestingly, when CRC cells were co-treated with NAC, the activation of JNK/c-Jun pathway induced by oridonin was nearly reversed, indicating that oridonin induced JNK/c-Jun pathway activation through the accumulation of ROS. Reactive Oxygen Species 223-226 mitogen-activated protein kinase 8 Homo sapiens 74-77 30981511-8 2019 Interestingly, when CRC cells were co-treated with NAC, the activation of JNK/c-Jun pathway induced by oridonin was nearly reversed, indicating that oridonin induced JNK/c-Jun pathway activation through the accumulation of ROS. Reactive Oxygen Species 223-226 mitogen-activated protein kinase 8 Homo sapiens 166-169 31551215-5 2019 Furthermore, reactive oxygen species (ROS) stimulated the phosphorylation of ERK, p38 and JNK, while pre-administration of quercetin significantly (P<0.05) reduced the phosphorylation. Reactive Oxygen Species 13-36 mitogen-activated protein kinase 8 Homo sapiens 90-93 30857202-4 2019 In this study, we found that ferrous ammonium sulfate (FeAS), induced growth arrest and apoptosis in immature hematopoietic cells, which was mediated via reactive oxygen species (ROS) activation of p38MAPK and JNK pathways. Reactive Oxygen Species 179-182 mitogen-activated protein kinase 8 Homo sapiens 210-213 31396402-8 2019 Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 148-151 31396402-9 2019 Taken together, these results suggest a critical role for the ROS/ASK1/JNK pathway in the anticancer activity of pristimerin. Reactive Oxygen Species 62-65 mitogen-activated protein kinase 8 Homo sapiens 71-74 31122040-5 2019 Moreover, in bystander cells, APS inhibits expression of transforming growth factor beta receptor II (TGF- beta R II), a cell membrane receptor, resulting in lower ROS production and secretion via TGF- beta R-JNK/ERK-COX-2/ROS not P38 signaling. Reactive Oxygen Species 164-167 mitogen-activated protein kinase 8 Homo sapiens 209-212 30581004-10 2019 Importantly, suppressing ROS production abolished NHERF1 knockdown-induced JNK activation. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Homo sapiens 75-78 30338935-0 2019 Cardiac-specific Mst1 deficiency inhibits ROS-mediated JNK signalling to alleviate Ang II-induced cardiomyocyte apoptosis. Reactive Oxygen Species 42-45 mitogen-activated protein kinase 8 Homo sapiens 55-58 30338935-5 2019 In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Reactive Oxygen Species 191-194 mitogen-activated protein kinase 8 Homo sapiens 263-286 30338935-5 2019 In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Reactive Oxygen Species 191-194 mitogen-activated protein kinase 8 Homo sapiens 288-291 30338935-7 2019 Thus, cardiac-specific Mst1 knockout inhibits ROS-mediated JNK signalling to block Ang II-induced cardiomyocyte apoptosis, suggesting Mst1 as a potential therapeutic target for treatment of RAAS-activated heart failure. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 59-62 31582606-5 2019 In this review, we focus on a ROS-responsive protein kinase apoptosis signal-regulating kinase 1 (ASK1) that belongs to the mitogen-activated protein (MAP) kinase kinase kinase (MAP3K) family, and activates the c-jun N-terminal kinase (JNK) and p38 MAP kinase pathways, which consequently induces various cellular responses, including apoptosis and inflammation. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Homo sapiens 211-234 31582606-5 2019 In this review, we focus on a ROS-responsive protein kinase apoptosis signal-regulating kinase 1 (ASK1) that belongs to the mitogen-activated protein (MAP) kinase kinase kinase (MAP3K) family, and activates the c-jun N-terminal kinase (JNK) and p38 MAP kinase pathways, which consequently induces various cellular responses, including apoptosis and inflammation. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Homo sapiens 236-239 30229288-4 2018 LysoPC-induced responses were mediated via the NADPH oxidase-derived reactive oxygen species-dependent JNK1/2 phosphorylation pathway, leading to NF-kappaB and FoxO1 activation. Reactive Oxygen Species 69-92 mitogen-activated protein kinase 8 Homo sapiens 103-107 31307587-6 2019 This inhibits the electron transport chain and leads to formation of reactive oxygen species, which induce the activation of redox-sensitive members of the MAP kinase family ultimately causing activation of c-Jun N terminal kinase, JNK. Reactive Oxygen Species 69-92 mitogen-activated protein kinase 8 Homo sapiens 232-235 30268863-13 2018 p38MAPK, JNK and HO-1 were activated after PDT treatment and the activation were reversed by adding ROS scavenger NAC. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 8 Homo sapiens 9-12 30268863-15 2018 DVDMs-PDT induced ROS generation in Eca-109 cells, and the generation of ROS activated p38MAPK and JNK. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Homo sapiens 99-102 31122040-5 2019 Moreover, in bystander cells, APS inhibits expression of transforming growth factor beta receptor II (TGF- beta R II), a cell membrane receptor, resulting in lower ROS production and secretion via TGF- beta R-JNK/ERK-COX-2/ROS not P38 signaling. Reactive Oxygen Species 223-226 mitogen-activated protein kinase 8 Homo sapiens 209-212 30463289-3 2018 Recently, a JNK-mitochondrial SH3-domain binding protein 5 (SH3BP5/SAB)-ROS activation loop has been elucidated, which is required to sustain JNK activity. Reactive Oxygen Species 72-75 mitogen-activated protein kinase 8 Homo sapiens 12-15 30463289-3 2018 Recently, a JNK-mitochondrial SH3-domain binding protein 5 (SH3BP5/SAB)-ROS activation loop has been elucidated, which is required to sustain JNK activity. Reactive Oxygen Species 72-75 mitogen-activated protein kinase 8 Homo sapiens 142-145 30463289-5 2018 SAB is a docking protein and substrate for JNK, leading to an intramitochondrial signal transduction pathway, which impairs electron transport and promotes reactive oxygen species (ROS) release to sustain the MAPK cascade. Reactive Oxygen Species 156-179 mitogen-activated protein kinase 8 Homo sapiens 43-46 30463289-5 2018 SAB is a docking protein and substrate for JNK, leading to an intramitochondrial signal transduction pathway, which impairs electron transport and promotes reactive oxygen species (ROS) release to sustain the MAPK cascade. Reactive Oxygen Species 181-184 mitogen-activated protein kinase 8 Homo sapiens 43-46 30405817-7 2018 The introduction of ROS and JNK inhibitors suppressed hyperthermia-induced apoptosis in GEM-treated cells, suggesting that hyperthermia increased GEM cytotoxicity in PC SW1990 cells by inducing apoptosis via the ROS/JNK signaling pathway. Reactive Oxygen Species 20-23 mitogen-activated protein kinase 8 Homo sapiens 216-219 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 8 Homo sapiens 109-112 30066915-7 2018 In conclusion, GK demonstrated a neuroprotective effect on the simulated cerebral ischemia in vitro, and this effect was mediated through the inhibition of the mitochondria-mediated apoptosis pathway triggered by ROS-evoked p38 and JNK activation. Reactive Oxygen Species 213-216 mitogen-activated protein kinase 8 Homo sapiens 232-235 30274308-0 2018 Humanin Attenuates NMDA-Induced Excitotoxicity by Inhibiting ROS-dependent JNK/p38 MAPK Pathway. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 8 Homo sapiens 75-78 30274308-7 2018 Therefore, the present study suggests that inhibition of ROS-dependent JNK/p38 MAPK signaling pathway serves an effective strategy for HN neuroprotection against certain neurological diseases. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 8 Homo sapiens 71-74 30359319-14 2018 ROS/JNK signaling is essential in upregulating high glucose-induced autophagy. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 4-7 29627502-10 2018 Moreover, the ROS scavenger NAC prevented phosphorylation of both p38 and JNK. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 74-77 29847772-8 2018 Further mechanism study demonstrated that RA caused a significant enhance reactive oxygen species (ROS) level to stimulate phosphorylation of JNK. Reactive Oxygen Species 74-97 mitogen-activated protein kinase 8 Homo sapiens 142-145 29847772-8 2018 Further mechanism study demonstrated that RA caused a significant enhance reactive oxygen species (ROS) level to stimulate phosphorylation of JNK. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 8 Homo sapiens 142-145 29901107-0 2018 Autophagy protects bone marrow mesenchymal stem cells from palmitate-induced apoptosis through the ROS-JNK/p38 MAPK signaling pathways. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 8 Homo sapiens 103-106 29901107-10 2018 Therefore, the results indicated that PA can induce autophagy in BMSCs and protect cells from PA-induced apoptosis through the ROS-JNK/p38 MAPK signaling pathways. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 131-134 29602237-0 2018 NEFA-induced ROS impaired insulin signalling through the JNK and p38MAPK pathways in non-alcoholic steatohepatitis. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 57-60 29602237-4 2018 NEFA treatment significantly impaired mitochondrial function and, increased reactive oxygen species (ROS) production, and excessive ROS overactivated the JNK and p38MAPK pathways and induced insulin resistance in cow hepatocytes. Reactive Oxygen Species 132-135 mitogen-activated protein kinase 8 Homo sapiens 154-157 29602237-6 2018 These findings indicate that NEFAs induce mitochondrial dysfunction and insulin resistance mediated by the ROS-JNK/p38MAPK pathway. Reactive Oxygen Species 107-110 mitogen-activated protein kinase 8 Homo sapiens 111-114 29880532-8 2018 The higher ROS levels were responsible for the cell senescence, which was instigated by the p38-JNK-FOXO3a-p27 pathway. Reactive Oxygen Species 11-14 mitogen-activated protein kinase 8 Homo sapiens 96-99 29753743-0 2018 JLP-JNK signaling protects cancer cells from reactive oxygen species-induced cell death. Reactive Oxygen Species 45-68 mitogen-activated protein kinase 8 Homo sapiens 4-7 29753743-8 2018 These data collectively suggest that the JLP-JNK signaling pathway counteracts ROS-induced cancer cell death. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 45-48 29458150-9 2018 Moreover, treatment with 30 muM cisplatin elicited the formation of ROS, which, in turn, led to PINK1 activation, parkin recruitment, autophagy formation and JNK pathway relevant to apoptosis in HEI-OC1 cells, HCs, and SGNs. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 158-161 29805534-0 2018 Sonic hedgehog-c-Jun N-terminal kinase-zinc finger protein Gli1 signaling protects against high glucose concentration-induced reactive oxygen species generation in human fibroblasts. Reactive Oxygen Species 126-149 mitogen-activated protein kinase 8 Homo sapiens 15-38 29630880-0 2018 3"-Hydroxy-3,4"-dimethoxyflavone-induced cell death in human leukaemia cells is dependent on caspases and reactive oxygen species and attenuated by the inhibition of JNK/SAPK. Reactive Oxygen Species 106-129 mitogen-activated protein kinase 8 Homo sapiens 166-174 29458150-10 2018 Meanwhile, co-treatment with ROS scavenger N-acetyl-L-cysteine (NAC) or H2O2 consumer catalase-polyethylene glycol (PEG-catalase) inhibited parkin recruitment, alleviated autophagy formation, and mitigated JNK pathway related apoptosis. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 8 Homo sapiens 206-209 29609096-0 2018 Reactive oxygen species activate differentiation gene transcription of acute myeloid leukemia cells via the JNK/c-JUN signaling pathway. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 108-111 29568920-9 2018 Taken together, these findings indicate that Ordn induces the apoptosis of oral cancer cells probably via ROS-mediated JNK/p38 MAPK and mitochondrial pathways; thus, Ordn may have potential for use in the treatment of oral cancer. Reactive Oxygen Species 106-109 mitogen-activated protein kinase 8 Homo sapiens 119-122 29752466-9 2018 Furthermore, we confirmed that c-jun kinase (JNK) signal was involved in the inhibitory effect of miR-5591-5p on AGEs/AGER axis-induced ROS generation and apoptosis in ADSCs. Reactive Oxygen Species 136-139 mitogen-activated protein kinase 8 Homo sapiens 31-43 29752466-9 2018 Furthermore, we confirmed that c-jun kinase (JNK) signal was involved in the inhibitory effect of miR-5591-5p on AGEs/AGER axis-induced ROS generation and apoptosis in ADSCs. Reactive Oxygen Species 136-139 mitogen-activated protein kinase 8 Homo sapiens 45-48 29609096-8 2018 Moreover, we demonstrated that short ROS elevation mediated cell cycle arrest, but failed to activate myeloid gene transcription; whereas prolonged ROS elevation activated JNK/c-JUN signaling pathway. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Homo sapiens 172-175 29609096-10 2018 These findings provide new insights into the crucial role of JNK/c-Jun signaling pathway in the activation of transcriptional program during ROS-mediated AML differentiation. Reactive Oxygen Species 141-144 mitogen-activated protein kinase 8 Homo sapiens 61-64 28441795-7 2018 Furthermore, LPS-stimulated production of ROS, activation of NADPH oxidase and expression of inflammatory mediators were markedly suppressed by treatment with selective inhibitor of p38MAPK (SB203580) and JNK (SP600125). Reactive Oxygen Species 42-45 mitogen-activated protein kinase 8 Homo sapiens 205-208 29389802-9 2018 N-acetyl-L-cysteine, a scavenger of ROS, significantly reversed dioscin-induced cell death and activation of JNK and p38. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 109-112 29510199-10 2018 ROS scavenger N-acetyl-L-cysteine partially rescued HepG2 cell growth and prevented MPP depolarization, ERK and JNK activation. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 112-115 29389802-10 2018 Collectively, the data indicate that the induction of apoptosis by dioscin is mediated through ROS proteins, which are critical upstream signals for JNK/p38-MAPK activation. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 8 Homo sapiens 149-152 29291542-4 2018 Inhibitors of the c-JNK (SP600125) and p38-MAPK (SB203580) reduced lipopolysaccharide-caused production of inflammatory mediators, activation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes. Reactive Oxygen Species 185-208 mitogen-activated protein kinase 8 Homo sapiens 20-23 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 8 Homo sapiens 205-211 29348070-2 2018 Apoptosis signal-regulating kinase 1 (ASK1) has been reported to be activated by intracellular ROS and its inhibition leads to a down regulation of p38-and JNK-dependent signaling. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 8 Homo sapiens 156-159 29445146-6 2018 Meanwhile, we found that excessive ROS-activated JNK cascade to facilitate the ubiquitination and subsequent degradation of Gata4 protein. Reactive Oxygen Species 35-38 mitogen-activated protein kinase 8 Homo sapiens 49-52 29225132-0 2018 Ginsenoside Rh4 induces apoptosis and autophagic cell death through activation of the ROS/JNK/p53 pathway in colorectal cancer cells. Reactive Oxygen Species 86-89 mitogen-activated protein kinase 8 Homo sapiens 90-93 29705809-9 2018 And, we found high glucose-induced reactive oxygen species (ROS) promotes two signaling; JNK which regulates gamma-secretase leading to the cleavage of Notch proteins and PI3K/Akt signaling which enhances GSK-3beta phosphorylation. Reactive Oxygen Species 35-58 mitogen-activated protein kinase 8 Homo sapiens 89-92 29207156-6 2018 Intracellular ROS levels were significantly increased in the H2O2-treated cells at 1 and 24 h. Only the JNK inhibitor increased ROS levels in the H2O2-treated cells at 1 h and all MAPK inhibitors raised superoxide anion levels in these cells at 24 h. In addition, H2O2 induced GSH depletion in Calu-6 and A549 cells and the JNK inhibitor significantly enhanced GSH depletion in H2O2-treated cells. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 104-107 29207156-6 2018 Intracellular ROS levels were significantly increased in the H2O2-treated cells at 1 and 24 h. Only the JNK inhibitor increased ROS levels in the H2O2-treated cells at 1 h and all MAPK inhibitors raised superoxide anion levels in these cells at 24 h. In addition, H2O2 induced GSH depletion in Calu-6 and A549 cells and the JNK inhibitor significantly enhanced GSH depletion in H2O2-treated cells. Reactive Oxygen Species 128-131 mitogen-activated protein kinase 8 Homo sapiens 104-107 29940575-14 2018 CONCLUSIONS: Knockdown of miR-20a enhanced sensitivity of colorectal cancer cells to cisplatin through the ROS/ASK1/JNK pathway. Reactive Oxygen Species 107-110 mitogen-activated protein kinase 8 Homo sapiens 116-119 29705809-9 2018 And, we found high glucose-induced reactive oxygen species (ROS) promotes two signaling; JNK which regulates gamma-secretase leading to the cleavage of Notch proteins and PI3K/Akt signaling which enhances GSK-3beta phosphorylation. Reactive Oxygen Species 60-63 mitogen-activated protein kinase 8 Homo sapiens 89-92 28681938-0 2018 omega-hydroxyundec-9-enoic acid induces apoptosis by ROS mediated JNK and p38 phosphorylation in breast cancer cell lines. Reactive Oxygen Species 53-56 mitogen-activated protein kinase 8 Homo sapiens 66-69 28681938-8 2018 Collectively, omega-HUA-induced intracellular ROS generation induced breast cancer cell apoptosis through JNK and p38 signaling pathway activation, resulting in tumor regression. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 106-109 28815947-4 2017 Increased levels of reactive oxygen species (ROS) were also detected along with increased phosphorylation of the p38 and JNK. Reactive Oxygen Species 45-48 mitogen-activated protein kinase 8 Homo sapiens 121-124 28444898-14 2017 The induction of ROS upon HC6h treatment leads to the activation of JNK that mediates autophagy and apoptosis in human A549 cancer cells. Reactive Oxygen Species 17-20 mitogen-activated protein kinase 8 Homo sapiens 68-71 28815947-4 2017 Increased levels of reactive oxygen species (ROS) were also detected along with increased phosphorylation of the p38 and JNK. Reactive Oxygen Species 20-43 mitogen-activated protein kinase 8 Homo sapiens 121-124 28950661-7 2017 Reactive oxygen species (ROS) generation, up to 39.86+-2.32%, was also highly triggered by TRAIL and LIN combinational treatment, which was accompanied with high phosphorylation of c-Jun-N-terminal kinase (JNK). Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 181-204 29296219-0 2017 Coronarin D induces reactive oxygen species-mediated cell death in human nasopharyngeal cancer cells through inhibition of p38 MAPK and activation of JNK. Reactive Oxygen Species 20-43 mitogen-activated protein kinase 8 Homo sapiens 150-153 28923349-4 2017 Inhibitors of c-JNK (SP600125) and p38-MAPK (SB203580) attenuated the lipoteichoic acid- or peptidoglycan-induced production of inflammatory mediators, the activation of the JNK and p38-MAPK, and the production of reactive oxygen species in keratinocytes. Reactive Oxygen Species 214-237 mitogen-activated protein kinase 8 Homo sapiens 174-177 28950661-7 2017 Reactive oxygen species (ROS) generation, up to 39.86+-2.32%, was also highly triggered by TRAIL and LIN combinational treatment, which was accompanied with high phosphorylation of c-Jun-N-terminal kinase (JNK). Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 206-209 28950661-7 2017 Reactive oxygen species (ROS) generation, up to 39.86+-2.32%, was also highly triggered by TRAIL and LIN combinational treatment, which was accompanied with high phosphorylation of c-Jun-N-terminal kinase (JNK). Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Homo sapiens 181-204 28950661-7 2017 Reactive oxygen species (ROS) generation, up to 39.86+-2.32%, was also highly triggered by TRAIL and LIN combinational treatment, which was accompanied with high phosphorylation of c-Jun-N-terminal kinase (JNK). Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Homo sapiens 206-209 29268509-16 2017 Conclusions: PM exposure enhanced the airway inflammatory response significantly through ROS-mediated activation of MAPK (ERK, JNK, p38 MAPK) and downstream NF-kappaB signaling pathways. Reactive Oxygen Species 89-92 mitogen-activated protein kinase 8 Homo sapiens 127-130 28919046-8 2017 The resultant rise in intracellular calcium and production of mitochondrial reactive oxygen species induced expression of NFAT responsive-genes and enhanced TGF-beta1 autoinduction through non-canonical JNK-dependent pathways. Reactive Oxygen Species 76-99 mitogen-activated protein kinase 8 Homo sapiens 203-206 28849240-0 2017 Chaetocin induces cell cycle arrest and apoptosis by regulating the ROS-mediated ASK-1/JNK signaling pathways. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 87-90 28432555-0 2017 Rotundarpene inhibits TNF-alpha-induced activation of the Akt, mTOR, and NF-kappaB pathways, and the JNK and p38 associated with production of reactive oxygen species. Reactive Oxygen Species 143-166 mitogen-activated protein kinase 8 Homo sapiens 101-104 28849240-5 2017 These findings indicate that chaetocin arrests the cell cycle and induces apoptosis by regulating the reactive oxygen species-mediated ASK-1/JNK signaling pathways. Reactive Oxygen Species 102-125 mitogen-activated protein kinase 8 Homo sapiens 141-144 28801533-8 2017 In conclusion, Gli treatment significantly induced cell apoptosis by promoting ROS-dependent JNK pathway activation in HCC cells. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 93-96 28963507-3 2017 PRDX6 activation generates reactive oxygen species via NADPH oxidase, reducing the palmitoylation of receptor-associated Galphai in a JNK-dependent manner. Reactive Oxygen Species 27-50 mitogen-activated protein kinase 8 Homo sapiens 134-137 28801533-0 2017 Glibenclamide induces apoptosis by activating reactive oxygen species dependent JNK pathway in hepatocellular carcinoma cells. Reactive Oxygen Species 46-69 mitogen-activated protein kinase 8 Homo sapiens 80-83 28893319-0 2017 Sophoridine induces apoptosis and S phase arrest via ROS-dependent JNK and ERK activation in human pancreatic cancer cells. Reactive Oxygen Species 53-56 mitogen-activated protein kinase 8 Homo sapiens 67-70 28801533-6 2017 Scavenging of the intracellular ROS with its blocker N-acetyl-L-cysteine (NAC) could mitigate the Gli-induced apoptosis and JNK activation in the two HCC cell lines. Reactive Oxygen Species 32-35 mitogen-activated protein kinase 8 Homo sapiens 124-127 28891980-9 2017 Moreover, ROS activated autophagy via the Akt-mTOR and JNK pathways. Reactive Oxygen Species 10-13 mitogen-activated protein kinase 8 Homo sapiens 55-58 28871102-5 2017 Ang II decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-beta1 induction. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 8 Homo sapiens 147-150 29089080-1 2017 Objective To study the role of reactive oxygen species/c-Jun N-terminal kinase (ROS/JNK) pathway in apoptosis of human lung epithelial A549 cells induced by chrysotile from Sichuan Xinkang. Reactive Oxygen Species 31-54 mitogen-activated protein kinase 8 Homo sapiens 84-87 28715876-9 2017 Importantly, TRAIL/LIQ-triggered apoptosis and JNK were dependent on ROS production. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 8 Homo sapiens 47-50 28369600-8 2017 Since it has been shown that the inhibitor for JNK can suppress the radiation-induced upregulation of TLR expression, the present results suggest that ionizing radiation increased the cell surface expressions of TLR2 and TLR4 through reactive oxygen species-mediated JNK activation. Reactive Oxygen Species 234-257 mitogen-activated protein kinase 8 Homo sapiens 47-50 28369600-8 2017 Since it has been shown that the inhibitor for JNK can suppress the radiation-induced upregulation of TLR expression, the present results suggest that ionizing radiation increased the cell surface expressions of TLR2 and TLR4 through reactive oxygen species-mediated JNK activation. Reactive Oxygen Species 234-257 mitogen-activated protein kinase 8 Homo sapiens 267-270 29089080-8 2017 Compared with the same concentration of chrysotile, ROS inhibitor significantly inhibited cell apoptosis, decreased the level of ROS, reduced the degree of mitochondrial membrane potential, and down-regulated the expressions of p-JNK1, p-JNK2 and cleaved caspase-3 proteins. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Homo sapiens 230-234 29089080-9 2017 Conclusion Chrysotile from Sichuan Xinkang might induce the apoptosis of A549 cells via ROS/JNK pathway. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 8 Homo sapiens 92-95 28515304-0 2017 Reactive Oxygen Species-Mediated c-Jun NH2-Terminal Kinase Activation Contributes to Hepatitis B Virus X Protein-Induced Autophagy via Regulation of the Beclin-1/Bcl-2 Interaction. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 33-58 29100399-7 2017 Through transcriptome analysis, we identified reactive oxygen species (ROS)-activated JNK/AP-1 signaling as a major pathway mediating apoptosis of MDS-L cells by WFA. Reactive Oxygen Species 46-69 mitogen-activated protein kinase 8 Homo sapiens 86-89 29100399-7 2017 Through transcriptome analysis, we identified reactive oxygen species (ROS)-activated JNK/AP-1 signaling as a major pathway mediating apoptosis of MDS-L cells by WFA. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Homo sapiens 86-89 28758971-0 2017 Tricetin Induces Apoptosis of Human Leukemic HL-60 Cells through a Reactive Oxygen Species-Mediated c-Jun N-Terminal Kinase Activation Pathway. Reactive Oxygen Species 67-90 mitogen-activated protein kinase 8 Homo sapiens 100-123 28969050-9 2017 The ROS scavenger also blocked PP-induced G2/M phase arrest and the phosphorylation of JNK. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 87-90 28474156-13 2017 JNK inhibitor SP600125 reduced JNK phosphorylation, downregulated cleaved caspase-3 protein level, decreased AP-1 transcriptional activity and ROS level, and reduced the transcription and expression of TNF-alpha and IL-6, which improved ALI and cell apoptosis after paraquat poisoning. Reactive Oxygen Species 143-146 mitogen-activated protein kinase 8 Homo sapiens 0-3 28758971-9 2017 Moreover, an ROS scavenger, N-acetylcysteine (NAC), reversed tricetin-induced JNK activation and subsequent cell apoptosis. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 78-81 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Reactive Oxygen Species 260-283 mitogen-activated protein kinase 8 Homo sapiens 102-125 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Reactive Oxygen Species 260-283 mitogen-activated protein kinase 8 Homo sapiens 127-130 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Reactive Oxygen Species 285-288 mitogen-activated protein kinase 8 Homo sapiens 102-125 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Reactive Oxygen Species 285-288 mitogen-activated protein kinase 8 Homo sapiens 127-130 28515304-7 2017 Moreover, it was found that HBx treatment led to the generation of reactive oxygen species (ROS), and inhibition of ROS activity abrogated both JNK activation and autophagosome formation. Reactive Oxygen Species 116-119 mitogen-activated protein kinase 8 Homo sapiens 144-147 28515304-8 2017 Of importance, ROS-JNK signaling was also revealed to play an important role in HBV-induced autophagosome formation and subsequent HBV replication. Reactive Oxygen Species 15-18 mitogen-activated protein kinase 8 Homo sapiens 19-22 28515304-12 2017 Further data showed that ROS-JNK activation by HBx resulted in the release of beclin-1 from its association with Bcl-2 to form a complex with VPS34, thus enhancing autophagosome formation. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Homo sapiens 29-32 28515304-13 2017 Of importance, ROS-JNK signaling was also demonstrated to be critical for HBV replication via regulation of autophagy induction. Reactive Oxygen Species 15-18 mitogen-activated protein kinase 8 Homo sapiens 19-22 28414098-9 2017 Both calcium chelator BAPTA-AM and JNK inhibitor SP600125 could attenuate necroptotic features, including mitochondrial ROS elevation, mitochondrial depolarization, and ATP depletion. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 35-38 28609656-3 2017 Liver damage, reactive oxygen species (ROS) and paracrine tumor necrosis factor (Tnf) from Kupffer cells caused JNK-mediated cholangiocellular proliferation and oncogenic transformation. Reactive Oxygen Species 14-37 mitogen-activated protein kinase 8 Homo sapiens 112-115 28457938-9 2017 Here, we provide the first description of PARP-1-ATF4-MKP-1-JNK/p38 MAPK retrograde pathway, which is responsible for the regulation of mitochondrial integrity, ROS production and cell death in oxidative stress, and may represent a new mechanism of PARP in cancer therapy since cancer stem cells development is JNK-dependent. Reactive Oxygen Species 161-164 mitogen-activated protein kinase 8 Homo sapiens 60-63 28457938-9 2017 Here, we provide the first description of PARP-1-ATF4-MKP-1-JNK/p38 MAPK retrograde pathway, which is responsible for the regulation of mitochondrial integrity, ROS production and cell death in oxidative stress, and may represent a new mechanism of PARP in cancer therapy since cancer stem cells development is JNK-dependent. Reactive Oxygen Species 161-164 mitogen-activated protein kinase 8 Homo sapiens 311-314 28473664-7 2017 CPPTL induced apoptosis of AML cells by stimulating ROS production, and accumulation of ROS then activated the JNK pathway, thereby promoting mitochondrial damage. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 8 Homo sapiens 111-114 28609656-3 2017 Liver damage, reactive oxygen species (ROS) and paracrine tumor necrosis factor (Tnf) from Kupffer cells caused JNK-mediated cholangiocellular proliferation and oncogenic transformation. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 8 Homo sapiens 112-115 28609656-8 2017 Targeting the ROS/Tnf/JNK axis may provide opportunities for ICC therapy. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 22-25 28111233-0 2017 CtBP2 ameliorates palmitate-induced insulin resistance in HepG2 cells through ROS mediated JNK pathway. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 8 Homo sapiens 91-94 28111233-10 2017 Thus, we demonstrated that CtBP2 ameliorated PA-induced insulin resistance via ROS-dependent JNK pathway. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 93-96 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 8 Homo sapiens 79-102 28393248-12 2017 ROS is known to serve a major role in high glucose induced-insulin resistance by increasing JNK and IRS1 serine phosphorylation. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 92-95 28393248-14 2017 EGCG ameliorated high glucose-induced insulin resistance in the hepatocytes by potentially decreasing ROS-induced JNK/IRS1/AKT/GSK signaling. Reactive Oxygen Species 102-105 mitogen-activated protein kinase 8 Homo sapiens 114-117 28374828-5 2017 Furthermore, we found that JNK activity is required to repress stress-induced reactive oxygen species (ROS) accumulation in both the coral Stylophora pistillata and human skin cells. Reactive Oxygen Species 78-101 mitogen-activated protein kinase 8 Homo sapiens 27-30 28374828-5 2017 Furthermore, we found that JNK activity is required to repress stress-induced reactive oxygen species (ROS) accumulation in both the coral Stylophora pistillata and human skin cells. Reactive Oxygen Species 103-106 mitogen-activated protein kinase 8 Homo sapiens 27-30 28374828-6 2017 We also show that inhibiting JNK activation under stress conditions leads to ROS accumulation, subsequent coral bleaching and cell death. Reactive Oxygen Species 77-80 mitogen-activated protein kinase 8 Homo sapiens 29-32 28119491-8 2017 Romidepsin + fenretinide activated p38 and JNK via ROS, and knockdown of p38 and JNK1 significantly decreased the synergistic cytotoxicity. Reactive Oxygen Species 51-54 mitogen-activated protein kinase 8 Homo sapiens 43-46 28410397-14 2017 Our data shows that EMBS targets a pathway that leads to increased ROS production as an early event that culminates in G2/M arrest and apoptosis by means of JNK-signaling in cancer cells. Reactive Oxygen Species 67-70 mitogen-activated protein kinase 8 Homo sapiens 157-160 27539140-0 2017 Suppression of reactive oxygen species-mediated ERK and JNK activation sensitizes dihydromyricetin-induced mitochondrial apoptosis in human non-small cell lung cancer. Reactive Oxygen Species 15-38 mitogen-activated protein kinase 8 Homo sapiens 56-59 28087840-9 2017 Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 102-105 28087840-9 2017 Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Homo sapiens 102-105 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 8 Homo sapiens 104-107 27886548-7 2017 Moreover, compound 81 induced lung cancer cells death by inhibiting NF-kappaB signaling pathway, and activated the JNK-mitochondrial apoptotic pathway by increasing reactive oxygen species (ROS) generation resulting in apoptosis. Reactive Oxygen Species 165-188 mitogen-activated protein kinase 8 Homo sapiens 115-118 28287190-8 2017 The findings from this work reveal that NLRX1 sensitizes HEI-OC1 cells to cisplatin-induced apoptosis via activation of ROS/JNK signaling pathway, suggesting that NLRX1 acts as an important regulator of the cisplatin-elicited ototoxity. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 124-127 28151469-4 2017 In this study, we found that the accumulation of reactive oxygen species (ROS) by UVB irradiation was sufficient to trigger the activation of JNK and ERK mitogen-activated protein kinase (MAPK) in human primary epidermal keratinocytes. Reactive Oxygen Species 49-72 mitogen-activated protein kinase 8 Homo sapiens 142-145 28151469-4 2017 In this study, we found that the accumulation of reactive oxygen species (ROS) by UVB irradiation was sufficient to trigger the activation of JNK and ERK mitogen-activated protein kinase (MAPK) in human primary epidermal keratinocytes. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 142-145 28151469-9 2017 These data clearly indicated that BNIP3-induced autophagy, which occurs via UVB-generated ROS-mediated JNK and ERK MAPK activation, has a crucial role in the protection of the skin epidermis against UVB irradiation. Reactive Oxygen Species 90-93 mitogen-activated protein kinase 8 Homo sapiens 103-106 27988353-0 2017 The effects of urotensin II on migration and invasion are mediated by NADPH oxidase-derived reactive oxygen species through the c-Jun N-terminal kinase pathway in human hepatoma cells. Reactive Oxygen Species 92-115 mitogen-activated protein kinase 8 Homo sapiens 128-151 27988353-14 2017 CONCLUSIONS: Exogenous UII induced migration and invasion in hepatoma cells that mainly involved NADPH oxidase-derived ROS through JNK activation. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 8 Homo sapiens 131-134 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 8 Homo sapiens 140-163 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 8 Homo sapiens 165-168 26756900-0 2016 COX-2 inhibitor NS-398 suppresses doxorubicin-induced p53 accumulation through inhibition of ROS-mediated Jnk activation. Reactive Oxygen Species 93-96 mitogen-activated protein kinase 8 Homo sapiens 106-109 26822174-7 2016 Inhibitor experiments showed that PEITC induced apoptosis through ROS-mediated JNK activation and upregulation of DR4 and DR5. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Homo sapiens 79-82 26756900-10 2016 Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation. Reactive Oxygen Species 21-44 mitogen-activated protein kinase 8 Homo sapiens 103-106 26756900-10 2016 Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 103-106 26756900-12 2016 These results suggest that COX-2 activates Jnk through modulation of ROS levels, leading to accumulation of p53. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 8 Homo sapiens 43-46 27726288-0 2016 Erlotinib induces the human non-small-cell lung cancer cells apoptosis via activating ROS-dependent JNK pathways. Reactive Oxygen Species 86-89 mitogen-activated protein kinase 8 Homo sapiens 100-103 27779694-8 2016 In conclusion, fentanyl reduces the sensitivity of cisplatin in lung cancer cells through the ROS-JNK-autophagy pathway, whereas the autophagy inhibitor 3-MA may weaken this effect. Reactive Oxygen Species 94-97 mitogen-activated protein kinase 8 Homo sapiens 98-101 27726288-2 2016 So, the aim of this research was to explore the underlying anticancer mechanisms of ERL and to explore whether the reactive oxygen species (ROS)-dependent c-Jun N-terminal kinase (JNK) pathway contributed to the anticancer properties provided by ERL. Reactive Oxygen Species 115-138 mitogen-activated protein kinase 8 Homo sapiens 155-178 27726288-2 2016 So, the aim of this research was to explore the underlying anticancer mechanisms of ERL and to explore whether the reactive oxygen species (ROS)-dependent c-Jun N-terminal kinase (JNK) pathway contributed to the anticancer properties provided by ERL. Reactive Oxygen Species 115-138 mitogen-activated protein kinase 8 Homo sapiens 180-183 27726288-2 2016 So, the aim of this research was to explore the underlying anticancer mechanisms of ERL and to explore whether the reactive oxygen species (ROS)-dependent c-Jun N-terminal kinase (JNK) pathway contributed to the anticancer properties provided by ERL. Reactive Oxygen Species 140-143 mitogen-activated protein kinase 8 Homo sapiens 155-178 27726288-2 2016 So, the aim of this research was to explore the underlying anticancer mechanisms of ERL and to explore whether the reactive oxygen species (ROS)-dependent c-Jun N-terminal kinase (JNK) pathway contributed to the anticancer properties provided by ERL. Reactive Oxygen Species 140-143 mitogen-activated protein kinase 8 Homo sapiens 180-183 27726288-10 2016 As expected, intracellular ROS activated the proapoptotic JNK signaling pathway and inhibited the activation of EFGR signaling pathway. Reactive Oxygen Species 27-30 mitogen-activated protein kinase 8 Homo sapiens 58-61 27726288-15 2016 Our results suggest that ERL induces A549 cells apoptosis via activating ROS-dependent JNK pathways in human non-small lung cancer cells that provide a new experimental foundation for cancer therapy. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Homo sapiens 87-90 27667173-0 2016 Combined oridonin with cetuximab treatment shows synergistic anticancer effects on laryngeal squamous cell carcinoma: involvement of inhibition of EGFR and activation of reactive oxygen species-mediated JNK pathway. Reactive Oxygen Species 170-193 mitogen-activated protein kinase 8 Homo sapiens 203-206 27667173-6 2016 Moreover, combination treatment caused cell death associated with suppression of p-EGFR and activation of reactive oxygen species (ROS)-mediated JNK pathway. Reactive Oxygen Species 106-129 mitogen-activated protein kinase 8 Homo sapiens 145-148 27667173-6 2016 Moreover, combination treatment caused cell death associated with suppression of p-EGFR and activation of reactive oxygen species (ROS)-mediated JNK pathway. Reactive Oxygen Species 131-134 mitogen-activated protein kinase 8 Homo sapiens 145-148 27754347-6 2016 Furthermore, we demonstrated that NJXA induced cell apoptosis by activating the reactive oxygen species (ROS)-mediated JNK signaling pathway. Reactive Oxygen Species 80-103 mitogen-activated protein kinase 8 Homo sapiens 119-122 27754347-6 2016 Furthermore, we demonstrated that NJXA induced cell apoptosis by activating the reactive oxygen species (ROS)-mediated JNK signaling pathway. Reactive Oxygen Species 105-108 mitogen-activated protein kinase 8 Homo sapiens 119-122 27398613-7 2016 Similarly, MAL-A mediated generation of ROS was decreased by inhibitors of p38MAPK and JNK, whereas the PI3K/AKT inhibitor potentiated its generation of ROS. Reactive Oxygen Species 40-43 mitogen-activated protein kinase 8 Homo sapiens 87-90 27532863-6 2016 This ROS-mediated activation of FOXO3 was dependent on mitogen-activated protein kinase 8 (MAPK8/JNK) activity. Reactive Oxygen Species 5-8 mitogen-activated protein kinase 8 Homo sapiens 55-89 27532863-6 2016 This ROS-mediated activation of FOXO3 was dependent on mitogen-activated protein kinase 8 (MAPK8/JNK) activity. Reactive Oxygen Species 5-8 mitogen-activated protein kinase 8 Homo sapiens 91-96 27532863-6 2016 This ROS-mediated activation of FOXO3 was dependent on mitogen-activated protein kinase 8 (MAPK8/JNK) activity. Reactive Oxygen Species 5-8 mitogen-activated protein kinase 8 Homo sapiens 97-100 27633119-8 2016 Taken together, the novel polysaccharide induced cancer cell apoptosis and arrested cell cycle via ROS/JNK signaling pathway. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 8 Homo sapiens 103-106 27633119-0 2016 A novel polysaccharide derived from algae extract induces apoptosis and cell cycle arrest in human gastric carcinoma MKN45 cells via ROS/JNK signaling pathway. Reactive Oxygen Species 133-136 mitogen-activated protein kinase 8 Homo sapiens 137-140 27570977-6 2016 Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK. Reactive Oxygen Species 28-51 mitogen-activated protein kinase 8 Homo sapiens 279-282 27466285-2 2016 Our previous studies have shown that life-span and antitumor function of T cells can be enhanced by inhibiting reactive oxygen species (ROS) or intervening with ROS-dependent JNK activation that leads to its activation-induced cell death. Reactive Oxygen Species 161-164 mitogen-activated protein kinase 8 Homo sapiens 175-178 27570977-6 2016 Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK. Reactive Oxygen Species 53-56 mitogen-activated protein kinase 8 Homo sapiens 279-282 26803514-5 2016 We also found that iron chelators induced reactive oxygen species (ROS) production, resulting in the activation of both c-Jun N-terminal kinase (JNK) and endoplasmic reticulum (ER) stress apoptotic pathways in gastric cancer cells. Reactive Oxygen Species 67-70 mitogen-activated protein kinase 8 Homo sapiens 120-143 27570977-7 2016 Taken together, these findings revealed that Vitamin K2 induces apoptosis in bladder cancer cells via ROS-mediated JNK/p38 MAPK and Mitochondrial pathways. Reactive Oxygen Species 102-105 mitogen-activated protein kinase 8 Homo sapiens 115-118 27248323-4 2016 Our results demonstrated that ROS-dependent activation of p38, JNK1/2 and Notch3 promoted basal and TGF-beta1-induced differentiation and expression of extracellular matrix proteins. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Homo sapiens 63-69 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 8 Homo sapiens 111-117 27176794-15 2016 The ROS scavenger also prevented phosphorylation of the JNK and p38 signaling pathway. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 56-59 27176794-16 2016 Our research proved that cinobufagin triggered apoptosis and autophagic cell death via activation of the ROS/JNK/p-38 axis. Reactive Oxygen Species 105-108 mitogen-activated protein kinase 8 Homo sapiens 109-112 28076833-8 2017 Furthermore, NAC (ROS inhibitor) could rescue GQ-induced cell death, reduce ROS generation, decrease the phosphorylation of p38 and JNK, and then attenuate the activation of mitochondrial signal pathway. Reactive Oxygen Species 18-21 mitogen-activated protein kinase 8 Homo sapiens 132-135 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 8 Homo sapiens 82-85 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 8 Homo sapiens 180-183 27109479-11 2016 Our results suggest that UTI exerts its anti-oxidant effects by decreasing overproduction of ROS induced by LPS via suppressing JNK/c-Jun phosphorylation. Reactive Oxygen Species 93-96 mitogen-activated protein kinase 8 Homo sapiens 128-131 27035222-0 2016 Aloe-emodin-mediated photodynamic therapy induces autophagy and apoptosis in human osteosarcoma cell line MG-63 through the ROS/JNK signaling pathway. Reactive Oxygen Species 124-127 mitogen-activated protein kinase 8 Homo sapiens 128-131 27035222-8 2016 ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 115-118 27035222-8 2016 ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 124-127 27035222-9 2016 In conclusion, AE-PDT induced the autophagy and apoptosis of human osteosarcoma cell line MG-63 through the activation of the ROS-JNK signaling pathway. Reactive Oxygen Species 126-129 mitogen-activated protein kinase 8 Homo sapiens 130-133 27074555-6 2016 Interestingly, the ROS scavenger NAC attenuated carfilzomib/vorinostat-mediated activation of p38MAPK and JNK. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 8 Homo sapiens 106-109 27133064-5 2016 All those effects are contributed by reactive oxygen species (ROS) generation and ER stress-induced mitochondrial dysfunction which are also responsible for c-Jun N-terminal kinase (JNK) activation. Reactive Oxygen Species 37-60 mitogen-activated protein kinase 8 Homo sapiens 157-180 27133064-5 2016 All those effects are contributed by reactive oxygen species (ROS) generation and ER stress-induced mitochondrial dysfunction which are also responsible for c-Jun N-terminal kinase (JNK) activation. Reactive Oxygen Species 37-60 mitogen-activated protein kinase 8 Homo sapiens 182-185 27133064-5 2016 All those effects are contributed by reactive oxygen species (ROS) generation and ER stress-induced mitochondrial dysfunction which are also responsible for c-Jun N-terminal kinase (JNK) activation. Reactive Oxygen Species 62-65 mitogen-activated protein kinase 8 Homo sapiens 157-180 27133064-5 2016 All those effects are contributed by reactive oxygen species (ROS) generation and ER stress-induced mitochondrial dysfunction which are also responsible for c-Jun N-terminal kinase (JNK) activation. Reactive Oxygen Species 62-65 mitogen-activated protein kinase 8 Homo sapiens 182-185 27569089-0 2016 Anticancer activity of Honokiol against lymphoid malignant cells via activation of ROS-JNK and attenuation of Nrf2 and NF-kappaB. Reactive Oxygen Species 83-86 mitogen-activated protein kinase 8 Homo sapiens 87-90 27569089-1 2016 PURPOSE: To evaluate the effect of Honokiol (HK) in the ROS-JNK pro-apoptotic pathway and NF-kappaB, Nrf2 anti-apoptotic pathways, in order to seek a possible explanation for its anticancer efficacy. Reactive Oxygen Species 56-59 mitogen-activated protein kinase 8 Homo sapiens 60-63 27569089-12 2016 Furthermore, in the presence of ROS inhibitor NAC (10mM) for 24 hrs, the JNK pathway was markedly activated, together with inhibition of NF-kappaB activity and a reduced level of Nrf2 expression. Reactive Oxygen Species 32-35 mitogen-activated protein kinase 8 Homo sapiens 73-76 27116119-7 2016 These results show that ROS generation by HMF was the crucial mediator behind ER stress induction, resulting in intracellular Ca2+ release, JNK phosphorylation, and activation of the mitochondrial apoptosis pathway. Reactive Oxygen Species 24-27 mitogen-activated protein kinase 8 Homo sapiens 140-143 27116119-10 2016 These results were further confirmed by pre-treatment with the ROS scavenger N-acetyl-l-cysteine (NAC), which completely reversed the effects of HMF treatment by preventing lipid peroxidation, followed by abolishment of JNK phosphorylation and attenuation of apoptogenic marker proteins. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 8 Homo sapiens 220-223 26803514-5 2016 We also found that iron chelators induced reactive oxygen species (ROS) production, resulting in the activation of both c-Jun N-terminal kinase (JNK) and endoplasmic reticulum (ER) stress apoptotic pathways in gastric cancer cells. Reactive Oxygen Species 67-70 mitogen-activated protein kinase 8 Homo sapiens 145-148 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 8 Homo sapiens 230-233 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 8 Homo sapiens 35-38 26927933-8 2016 ROS, ER stress, NFkappaB, and TGF-beta1 signaling were blocked by JNK specific siRNA. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 66-69 26820294-0 2016 Downregulation of TFAM inhibits the tumorigenesis of non-small cell lung cancer by activating ROS-mediated JNK/p38MAPK signaling and reducing cellular bioenergetics. Reactive Oxygen Species 94-97 mitogen-activated protein kinase 8 Homo sapiens 107-110 26820294-3 2016 Herein, we report that downregulation of TFAM in NSCLC cells resulted in cell cycle arrest at G1 phase and significantly blocked NSCLC cell growth and migration through the activation of reactive oxygen species (ROS)-induced c-Jun amino-terminal kinase(JNK)/p38 MAPK signaling and decreased cellular bioenergetics. Reactive Oxygen Species 187-210 mitogen-activated protein kinase 8 Homo sapiens 253-256 26820294-3 2016 Herein, we report that downregulation of TFAM in NSCLC cells resulted in cell cycle arrest at G1 phase and significantly blocked NSCLC cell growth and migration through the activation of reactive oxygen species (ROS)-induced c-Jun amino-terminal kinase(JNK)/p38 MAPK signaling and decreased cellular bioenergetics. Reactive Oxygen Species 212-215 mitogen-activated protein kinase 8 Homo sapiens 253-256 26762228-7 2016 DHEA stimulates reactive oxygen species-independent jun N-terminal kinase (JNK) phosphoactivation and the treatment with JNK inhibitor reduces p62 mRNA levels, as well as DHEA-induced ACD. Reactive Oxygen Species 16-39 mitogen-activated protein kinase 8 Homo sapiens 52-73 26762228-7 2016 DHEA stimulates reactive oxygen species-independent jun N-terminal kinase (JNK) phosphoactivation and the treatment with JNK inhibitor reduces p62 mRNA levels, as well as DHEA-induced ACD. Reactive Oxygen Species 16-39 mitogen-activated protein kinase 8 Homo sapiens 75-78 26625208-7 2016 The generation of ROS in response to TMZ-POH seems to play a crucial role in the cell death process since the blockage of ROS production using the antioxidant N-acetyl-L-cysteine or catalase reversed the TMZ-POH-induced JNK activation, DNA damage, and cancer cell apoptosis. Reactive Oxygen Species 18-21 mitogen-activated protein kinase 8 Homo sapiens 220-223 26851027-4 2016 The specificity of ROS-mediated ATM-JNK activation was confirmed by treatment with N-acetylcysteine, a ROS scavenger. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 8 Homo sapiens 36-39 26851027-4 2016 The specificity of ROS-mediated ATM-JNK activation was confirmed by treatment with N-acetylcysteine, a ROS scavenger. Reactive Oxygen Species 103-106 mitogen-activated protein kinase 8 Homo sapiens 36-39 26851027-0 2016 ER-Dependent Ca++-mediated Cytosolic ROS as an Effector for Induction of Mitochondrial Apoptotic and ATM-JNK Signal Pathways in Gallic Acid-treated Human Oral Cancer Cells. Reactive Oxygen Species 37-40 mitogen-activated protein kinase 8 Homo sapiens 105-108 26625208-7 2016 The generation of ROS in response to TMZ-POH seems to play a crucial role in the cell death process since the blockage of ROS production using the antioxidant N-acetyl-L-cysteine or catalase reversed the TMZ-POH-induced JNK activation, DNA damage, and cancer cell apoptosis. Reactive Oxygen Species 122-125 mitogen-activated protein kinase 8 Homo sapiens 220-223 27109156-9 2016 ROS-centered pathways (e.g. mitochondrial autophagy, MAPK and JNK) and transcription factor-related pathways (e.g. NF-[Formula: see text]B and HIF) are frequently utilized by these polysaccharides with or without the further involvement of inflammatory and death receptor pathways. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 62-65 26343144-11 2016 Our findings showed that CTS induced pro-death autophagy through activating JNK signaling mediated by increasing intracellular ROS production. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 76-79 26694167-6 2016 Baicalein-induced reactive oxygen species activated the ASK1/JNK pathway with subsequent expression of TAp63. Reactive Oxygen Species 18-41 mitogen-activated protein kinase 8 Homo sapiens 61-64 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 8 Homo sapiens 75-78 25559363-13 2016 Moreover, findings herein suggest that Nox5-derived ROS and subsequent depletion of PKCzeta and JNK inactivation play a critical role in modulating intracellular signaling cascades involved in the proliferation and survival of PCa cells. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Homo sapiens 96-99 26578520-8 2016 Enhanced pro-inflammatory cytokine production and JNK activity under hypoxia were prevented by inhibiting reactive oxygen species generation. Reactive Oxygen Species 106-129 mitogen-activated protein kinase 8 Homo sapiens 50-53 26415087-0 2016 Reactive oxygen species mediate oridonin-induced apoptosis through DNA damage response and activation of JNK pathway in diffuse large B cell lymphoma. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 105-108 26415087-3 2016 ROS abolition blocked ORI-induced apoptosis and attenuated the expression of phospho-histone H2AX and phospho-JNK, indicating that ROS-mediated DNA damage and JNK pathway activation were involved in ORI-induced apoptosis. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 110-113 26415087-3 2016 ROS abolition blocked ORI-induced apoptosis and attenuated the expression of phospho-histone H2AX and phospho-JNK, indicating that ROS-mediated DNA damage and JNK pathway activation were involved in ORI-induced apoptosis. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 159-162 26415087-3 2016 ROS abolition blocked ORI-induced apoptosis and attenuated the expression of phospho-histone H2AX and phospho-JNK, indicating that ROS-mediated DNA damage and JNK pathway activation were involved in ORI-induced apoptosis. Reactive Oxygen Species 131-134 mitogen-activated protein kinase 8 Homo sapiens 110-113 26535076-5 2015 H2O2-induced ROS increased the levels of phosphorylated p38 mitogen activated protein kinase (MAPK), Jun-N-terminal kinase (JNK), ataxia telangiectasia mutated (ATM), and p53, which were inhibited by lycopene pretreatment. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 101-122 26517353-0 2015 Fusarochromanone-induced reactive oxygen species results in activation of JNK cascade and cell death by inhibiting protein phosphatases 2A and 5. Reactive Oxygen Species 25-48 mitogen-activated protein kinase 8 Homo sapiens 74-77 26517353-5 2015 Furthermore, we observed that FC101-activated JNK pathway was attributed to induction of reactive oxygen species (ROS). Reactive Oxygen Species 89-112 mitogen-activated protein kinase 8 Homo sapiens 46-49 26517353-5 2015 Furthermore, we observed that FC101-activated JNK pathway was attributed to induction of reactive oxygen species (ROS). Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Homo sapiens 46-49 26517353-6 2015 Pretreatment with N-acetyl-L-cysteine (NAC), a ROS scavenger and antioxidant, suppressed FC101-induced activation of JNK and cell death. Reactive Oxygen Species 47-50 mitogen-activated protein kinase 8 Homo sapiens 117-120 26517353-9 2015 The results indicate that FC101-induced ROS inhibits PP2A and PP5, leading to activation of JNK pathway and consequently resulting in cell death. Reactive Oxygen Species 40-43 mitogen-activated protein kinase 8 Homo sapiens 92-95 26664142-10 2015 ROS induced JNK activation and Akt downregulation in HCC cells. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 12-15 26549640-3 2015 Inhibition of NADPH oxidases or knockdown of gp91phox in CD8(+) T cells abrogates ROS generation, which in turn modulates JNK and NFkappaB signalling with decreases in both IFNgamma levels and CD39 expression. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 122-125 26535076-5 2015 H2O2-induced ROS increased the levels of phosphorylated p38 mitogen activated protein kinase (MAPK), Jun-N-terminal kinase (JNK), ataxia telangiectasia mutated (ATM), and p53, which were inhibited by lycopene pretreatment. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 124-127 26086160-0 2015 Reactive oxygen species mediate nitric oxide production through ERK/JNK MAPK signaling in HAPI microglia after PFOS exposure. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 68-71 26416447-12 2015 These highlighted that Hic-5 plays a central role in the positive feedback ROS-JNK signal cascade. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 8 Homo sapiens 79-82 26416447-14 2015 In conclusion, Hic-5 mediates ROS-JNK signaling and may serve as a therapeutic target for prevention of HCC progression. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Homo sapiens 34-37 26164795-10 2015 Besides, the MAPK, the downstream effect of reactive oxygen species accumulation including JNK could be activated by III-10, as well as the inactivation of ERK. Reactive Oxygen Species 44-67 mitogen-activated protein kinase 8 Homo sapiens 91-94 26463477-6 2015 ROS toxicity was associated with autophagy induction or JNK pathway activation which represented potential mechanisms of cell death induced by PRIMA-1(MET) in STS. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 56-59 26307448-5 2015 Although LPS/ATP did not activate inflammasome in RAW264.7 macrophages, it caused the ROS-dependent c-Jun N-terminal kinase1/2 (JNK1/2) activation and an associated lactate dehydrogenase (LDH) release in RAW264.7 macrophages, an indication of cytotoxicity. Reactive Oxygen Species 86-89 mitogen-activated protein kinase 8 Homo sapiens 100-126 26307448-5 2015 Although LPS/ATP did not activate inflammasome in RAW264.7 macrophages, it caused the ROS-dependent c-Jun N-terminal kinase1/2 (JNK1/2) activation and an associated lactate dehydrogenase (LDH) release in RAW264.7 macrophages, an indication of cytotoxicity. Reactive Oxygen Species 86-89 mitogen-activated protein kinase 8 Homo sapiens 128-134 26296767-3 2015 In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis. Reactive Oxygen Species 292-315 mitogen-activated protein kinase 8 Homo sapiens 230-233 26296767-3 2015 In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis. Reactive Oxygen Species 317-320 mitogen-activated protein kinase 8 Homo sapiens 230-233 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. Reactive Oxygen Species 146-149 mitogen-activated protein kinase 8 Homo sapiens 150-153 26296767-8 2015 Taken together, these observations suggest that HCV-induced ROS/JNK signalling transcriptionally activates Bim expression, which leads to Bax activation and apoptosis induction. Reactive Oxygen Species 60-63 mitogen-activated protein kinase 8 Homo sapiens 64-67 25042557-0 2015 Reactive oxygen species-dependent JNK downregulated olaquindox-induced autophagy in HepG2 cells. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 34-37 25980575-9 2015 Western blot analysis revealed that CdCl2 stimulated expression of c-jun N-terminal kinase (JNK) phosphorylation and the stimulation were inhibited by NAC, indicating the induction of JNK phosphorylation was stimulated following ROS production. Reactive Oxygen Species 229-232 mitogen-activated protein kinase 8 Homo sapiens 67-90 25980575-9 2015 Western blot analysis revealed that CdCl2 stimulated expression of c-jun N-terminal kinase (JNK) phosphorylation and the stimulation were inhibited by NAC, indicating the induction of JNK phosphorylation was stimulated following ROS production. Reactive Oxygen Species 229-232 mitogen-activated protein kinase 8 Homo sapiens 92-95 25980575-9 2015 Western blot analysis revealed that CdCl2 stimulated expression of c-jun N-terminal kinase (JNK) phosphorylation and the stimulation were inhibited by NAC, indicating the induction of JNK phosphorylation was stimulated following ROS production. Reactive Oxygen Species 229-232 mitogen-activated protein kinase 8 Homo sapiens 184-187 25858818-9 2015 Our results indicated that NOX4-derived ROS play pivotal roles in activating Src kinase activity leading to the activation of canonical (Smad3) and noncanonical (JNK) cascades that cooperate to attain maximum CCN2 expression. Reactive Oxygen Species 40-43 mitogen-activated protein kinase 8 Homo sapiens 162-165 26244039-0 2015 Pachymic acid induces apoptosis via activating ROS-dependent JNK and ER stress pathways in lung cancer cells. Reactive Oxygen Species 47-50 mitogen-activated protein kinase 8 Homo sapiens 61-64 26244039-11 2015 Moreover, blockage of ROS production reversed PA-induced JNK and ER stress activation. Reactive Oxygen Species 22-25 mitogen-activated protein kinase 8 Homo sapiens 57-60 25649257-12 2015 It is concluded from the above mentioned results that JNK/Nrf2 signal pathway is involved in the regulation of UBE1L via intracellular ROS status when cells came in contact with polyphenols. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 8 Homo sapiens 54-57 25042557-12 2015 Olaquindox-induced autophagy in HepG2 cells is upregulated by Beclin 1 but downregulated by ROS-dependent JNK. Reactive Oxygen Species 92-95 mitogen-activated protein kinase 8 Homo sapiens 106-109 25042557-10 2015 Meanwhile, JNK activation was remarkably blocked by NAC, indicating that ROS may be the upstream signaling molecules of JNK activation and involved in the negative regulation of olaquindox-induced autophagy. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Homo sapiens 11-14 25042557-10 2015 Meanwhile, JNK activation was remarkably blocked by NAC, indicating that ROS may be the upstream signaling molecules of JNK activation and involved in the negative regulation of olaquindox-induced autophagy. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Homo sapiens 120-123 26078726-0 2015 bFGF Promotes the Migration of Human Dermal Fibroblasts under Diabetic Conditions through Reactive Oxygen Species Production via the PI3K/Akt-Rac1- JNK Pathways. Reactive Oxygen Species 90-113 mitogen-activated protein kinase 8 Homo sapiens 148-151 25912909-0 2015 The switch from ER stress-induced apoptosis to autophagy via ROS-mediated JNK/p62 signals: A survival mechanism in methotrexate-resistant choriocarcinoma cells. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 8 Homo sapiens 74-77 25912909-6 2015 Further experiments demonstrated that this cell death switch was regulated by ROS-mediated JNK/p62 pathway and subsequently lead to the resistance of choriocarcinoma cells to methotrexate treatment. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 8 Homo sapiens 91-94 25912909-7 2015 CONCLUSIONS: This study provides evidence to explain a survival mechanism of the switch from ER stress-induced apoptosis to autophagy via ROS-mediated JNK/p62 signals in methotrexate-resistant choriocarcinoma cells and may implicate the chemotherapy of methotrexate resistance in choriocarcinoma. Reactive Oxygen Species 138-141 mitogen-activated protein kinase 8 Homo sapiens 151-154 25982794-7 2015 Inhibition of ROS generation by N-acetyl-l-cysteine (NAC) significantly prevented CBG-induced ERK, JNK and p38 MAPK activation and apoptosis. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 99-102 25982794-10 2015 Taken together, these findings suggest that CBG can act as a potent anticancer agent against MM and possibly exerts its effects through the ROS-mediated activation of ERK, JNK and p38 MAPK leading to the activation of caspase-3 in U266 cells. Reactive Oxygen Species 140-143 mitogen-activated protein kinase 8 Homo sapiens 172-175 26078726-8 2015 Therefore, our data suggested that bFGF promotes the migration of human dermal fibroblasts under diabetic conditions through increased ROS production via the PI3K/Akt-Rac1-JNK pathways. Reactive Oxygen Species 135-138 mitogen-activated protein kinase 8 Homo sapiens 172-175 25781201-7 2015 In sensitive breast cancer cells, 5F 203 activated ROS-responsive kinases: c-Jun-N-terminal kinase (JNK) and p38 mitogen activated protein kinase (p38). Reactive Oxygen Species 51-54 mitogen-activated protein kinase 8 Homo sapiens 75-98 25996379-0 2015 A Central Role for JNK/AP-1 Pathway in the Pro-Oxidant Effect of Pyrrolidine Dithiocarbamate through Superoxide Dismutase 1 Gene Repression and Reactive Oxygen Species Generation in Hematopoietic Human Cancer Cell Line U937. Reactive Oxygen Species 144-167 mitogen-activated protein kinase 8 Homo sapiens 19-22 25996379-11 2015 Taken together, these results suggest that PDTC acts as pro-oxidant compound in JNK/AP-1 dependent-manner by repressing the superoxide dismutase 1 gene leading to intracellular ROS accumulation. Reactive Oxygen Species 177-180 mitogen-activated protein kinase 8 Homo sapiens 80-83 25781201-12 2015 Our data demonstrate 5F 203 induces ROS-mediated DNA damage at least in part via AhR, JNK, or p38 activation and modulates the expression of oxidative stress-responsive genes such as cytoglobin to confer its anticancer action. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 86-89 25781201-7 2015 In sensitive breast cancer cells, 5F 203 activated ROS-responsive kinases: c-Jun-N-terminal kinase (JNK) and p38 mitogen activated protein kinase (p38). Reactive Oxygen Species 51-54 mitogen-activated protein kinase 8 Homo sapiens 100-103 25781201-9 2015 Pharmacological inhibition of AhR, JNK, or p38 attenuated 5F 203-mediated increases in intracellular ROS, apoptosis, and single-strand break formation. Reactive Oxygen Species 101-104 mitogen-activated protein kinase 8 Homo sapiens 35-38 25178491-0 2015 2-(Pro-1-ynyl)-5-(5,6-dihydroxypenta-1,3-diynyl) thiophene induces apoptosis through reactive oxygen species-mediated JNK activation in human colon cancer SW620 cells. Reactive Oxygen Species 85-108 mitogen-activated protein kinase 8 Homo sapiens 118-121 25714022-0 2015 ROS generation mediates the anti-cancer effects of WZ35 via activating JNK and ER stress apoptotic pathways in gastric cancer. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 71-74 25714022-6 2015 Blockage of ROS production totally reversed WZ35-induced JNK and ER stress activation as well as cancer cell apoptosis. Reactive Oxygen Species 12-15 mitogen-activated protein kinase 8 Homo sapiens 57-60 25607831-0 2015 CDK5RAP1 deficiency induces cell cycle arrest and apoptosis in human breast cancer cell line by the ROS/JNK signaling pathway. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 8 Homo sapiens 104-107 25607831-8 2015 Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells. Reactive Oxygen Species 60-63 mitogen-activated protein kinase 8 Homo sapiens 158-161 25607831-9 2015 Taken together, these data indicated that CDK5RAP1 deficiency induced cell cycle arrest and apoptosis in human breast cancer MCF-7 cells by the ROS/JNK signaling pathway. Reactive Oxygen Species 144-147 mitogen-activated protein kinase 8 Homo sapiens 148-151 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 8 Homo sapiens 121-124 25352028-6 2015 In both MCF-7 and MDA-MB-231 cells, berberine increased the production of reactive oxygen species (ROS), which activated the pro-apoptotic JNK signaling. Reactive Oxygen Species 74-97 mitogen-activated protein kinase 8 Homo sapiens 139-142 25352028-6 2015 In both MCF-7 and MDA-MB-231 cells, berberine increased the production of reactive oxygen species (ROS), which activated the pro-apoptotic JNK signaling. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 8 Homo sapiens 139-142 26073866-5 2015 Activation of the JNK pathway induced by ROS was also reduced by azelnidipine. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 8 Homo sapiens 18-21 25473894-0 2015 JNK suppression of chemotherapeutic agents-induced ROS confers chemoresistance on pancreatic cancer stem cells. Reactive Oxygen Species 51-54 mitogen-activated protein kinase 8 Homo sapiens 0-3 25876967-1 2015 OBJECTIVE: This study will explore whether reactive oxygen species (ROS) is involved in TGF-beta1-induced JNK activation, pulmonary fibroblast proliferation and collagen type I and III synthesis. Reactive Oxygen Species 43-66 mitogen-activated protein kinase 8 Homo sapiens 106-109 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Reactive Oxygen Species 87-110 mitogen-activated protein kinase 8 Homo sapiens 15-18 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Reactive Oxygen Species 112-115 mitogen-activated protein kinase 8 Homo sapiens 15-18 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Reactive Oxygen Species 147-150 mitogen-activated protein kinase 8 Homo sapiens 15-18 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Reactive Oxygen Species 147-150 mitogen-activated protein kinase 8 Homo sapiens 187-190 25473894-6 2015 Our findings thus suggest that JNK may contribute to the chemoresistance of pancreatic CSCs through prevention of chemotherapeutic agents-induced increase in intracellular ROS. Reactive Oxygen Species 172-175 mitogen-activated protein kinase 8 Homo sapiens 31-34 25876967-1 2015 OBJECTIVE: This study will explore whether reactive oxygen species (ROS) is involved in TGF-beta1-induced JNK activation, pulmonary fibroblast proliferation and collagen type I and III synthesis. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 106-109 25876967-6 2015 CONCLUSION: TGF-beta1 induces pulmonary fibroblasts to generate ROS, which contributes to JNK activation and pulmonary fibroblast proliferation as well as collagen synthesis, while ROS inhibition suppresses this effet of TGF-beta1 in pulmonary fibroblasts. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 90-93 25323903-10 2014 Apoptosis of SW1763 as well as expressions of elevated phosphor-JNK, phosphor-p38, and caspase-3 induced by NTP were effectively inhibited by intracellular ROS scavengers. Reactive Oxygen Species 156-159 mitogen-activated protein kinase 8 Homo sapiens 64-67 25526030-4 2014 Here, we found that Lon expression in bladder cancer tissues was significantly higher than those in noncancerous tissues; down-regulation of Lon in bladder cancer cells significantly blocked cancer cell proliferation via suppression c-Jun N-terminal kinase (JNK) phosphorylation due to decreased reactive oxygen species (ROS) production and enhanced the sensitivity of bladder cancer cells to chemotherapeutic agents by promoting apoptosis. Reactive Oxygen Species 296-319 mitogen-activated protein kinase 8 Homo sapiens 258-261 25526030-4 2014 Here, we found that Lon expression in bladder cancer tissues was significantly higher than those in noncancerous tissues; down-regulation of Lon in bladder cancer cells significantly blocked cancer cell proliferation via suppression c-Jun N-terminal kinase (JNK) phosphorylation due to decreased reactive oxygen species (ROS) production and enhanced the sensitivity of bladder cancer cells to chemotherapeutic agents by promoting apoptosis. Reactive Oxygen Species 321-324 mitogen-activated protein kinase 8 Homo sapiens 258-261 25198898-0 2014 Curcumin induced human gastric cancer BGC-823 cells apoptosis by ROS-mediated ASK1-MKK4-JNK stress signaling pathway. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 8 Homo sapiens 88-91 25294812-0 2014 Ciclopirox induces autophagy through reactive oxygen species-mediated activation of JNK signaling pathway. Reactive Oxygen Species 37-60 mitogen-activated protein kinase 8 Homo sapiens 84-87 25294812-6 2014 However, only inhibition of JNK (with SP600125) or expression of dominant negative c-Jun partially prevented CPX-induced autophagy, indicating that ROS-mediated activation of JNK signaling pathway contributed to CPX-induced autophagy. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Homo sapiens 28-31 25294812-6 2014 However, only inhibition of JNK (with SP600125) or expression of dominant negative c-Jun partially prevented CPX-induced autophagy, indicating that ROS-mediated activation of JNK signaling pathway contributed to CPX-induced autophagy. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Homo sapiens 175-178 25181458-3 2014 Tetrandrine-induced cell death in prostate cancer cells is caused by reactive oxygen species (ROS)-mediated activation of c-Jun NH2-terminal kinase (JNK1/2). Reactive Oxygen Species 69-92 mitogen-activated protein kinase 8 Homo sapiens 149-155 25181458-3 2014 Tetrandrine-induced cell death in prostate cancer cells is caused by reactive oxygen species (ROS)-mediated activation of c-Jun NH2-terminal kinase (JNK1/2). Reactive Oxygen Species 94-97 mitogen-activated protein kinase 8 Homo sapiens 149-155 24875536-0 2014 Inhibition of cathepsin S induces autophagy and apoptosis in human glioblastoma cell lines through ROS-mediated PI3K/AKT/mTOR/p70S6K and JNK signaling pathways. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 8 Homo sapiens 137-140 24875536-5 2014 In addition, reactive oxygen species (ROS) served as an upstream of PI3K/AKT/mTOR/p70S6K and JNK signaling pathways. Reactive Oxygen Species 13-36 mitogen-activated protein kinase 8 Homo sapiens 93-96 24875536-5 2014 In addition, reactive oxygen species (ROS) served as an upstream of PI3K/AKT/mTOR/p70S6K and JNK signaling pathways. Reactive Oxygen Species 38-41 mitogen-activated protein kinase 8 Homo sapiens 93-96 24919794-9 2014 Hence, HMJ-30-induced endothelial cell apoptosis involved the ROS/JNK-regulated DR5 pathway. Reactive Oxygen Species 62-65 mitogen-activated protein kinase 8 Homo sapiens 66-69 24997392-9 2014 Inhibiting the ROS production using Nox4 siRNA or antagonizing ROS using GSH reduced cellular ROS level and attenuated AGE-induced GRP78 expression and IRE1alpha and JNK activation. Reactive Oxygen Species 15-18 mitogen-activated protein kinase 8 Homo sapiens 166-169 24359220-3 2014 RECENT ADVANCES: Low levels of ROS modify Atg4 and high mobility group box 1 (HMGB1) proteins, activate AMP-activated protein kinase (AMPK) and apoptosis signal-regulating kinase/c-Jun N-terminal kinase (JNK) pathways, or transactivate various proteins that could upregulate autophagy, leading to reductions in apoptosis. Reactive Oxygen Species 31-34 mitogen-activated protein kinase 8 Homo sapiens 204-207 24755146-7 2014 Using various inhibitors and antioxidant agents, we found that mitochondrial derived reactive oxygen species and depletion of mitochondrial transmembrane potential lead to the phosphorylation of p38 MAPK and JNK. Reactive Oxygen Species 85-108 mitogen-activated protein kinase 8 Homo sapiens 208-211 24333467-6 2014 One major pathway frequently involved in HC apoptosis is the c-jun N-terminal kinase (JNK) signaling pathway activated by reactive oxygen species, but other apoptotic pathways can also play a role in ototoxicity. Reactive Oxygen Species 122-145 mitogen-activated protein kinase 8 Homo sapiens 61-84 24911792-5 2014 Moreover, reactive oxygen species (ROS) generation and upregulation of both TAp73 and ER stress sensor proteins were detected after CD47 ligation, and p38 inhibitor SB203580 and JNK inhibitor SP600125 blocked upregulation of TAp73 and cell cycle arrest. Reactive Oxygen Species 10-33 mitogen-activated protein kinase 8 Homo sapiens 178-181 24911792-5 2014 Moreover, reactive oxygen species (ROS) generation and upregulation of both TAp73 and ER stress sensor proteins were detected after CD47 ligation, and p38 inhibitor SB203580 and JNK inhibitor SP600125 blocked upregulation of TAp73 and cell cycle arrest. Reactive Oxygen Species 35-38 mitogen-activated protein kinase 8 Homo sapiens 178-181 24333467-6 2014 One major pathway frequently involved in HC apoptosis is the c-jun N-terminal kinase (JNK) signaling pathway activated by reactive oxygen species, but other apoptotic pathways can also play a role in ototoxicity. Reactive Oxygen Species 122-145 mitogen-activated protein kinase 8 Homo sapiens 86-89 24878898-10 2014 In particular, the JNK-specific inhibitor SP600125 blocked KIOM-C-induced ROS generation and CHOP expression almost completely, which consequently almost completely rescued cell death, indicating that JNK activation plays a critical role in KIOM-C-induced cell death. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 19-22 24841907-7 2014 These results demonstrated for the first time that ISO simultaneously induced apoptosis and autophagy by ROS-related p53, PI3K/Akt, JNK, and p38 signaling pathways. Reactive Oxygen Species 105-108 mitogen-activated protein kinase 8 Homo sapiens 132-135 24612139-6 2014 Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins. Reactive Oxygen Species 93-96 mitogen-activated protein kinase 8 Homo sapiens 143-146 24680927-0 2014 Ziyuglycoside II induces cell cycle arrest and apoptosis through activation of ROS/JNK pathway in human breast cancer cells. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 83-86 24680927-6 2014 More importantly, the c-Jun NH2-terminal kinase (JNK), a downstream target of ROS, was found to be a critical mediator of ziyuglycoside II-induced cell apoptosis. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 8 Homo sapiens 22-47 24680927-6 2014 More importantly, the c-Jun NH2-terminal kinase (JNK), a downstream target of ROS, was found to be a critical mediator of ziyuglycoside II-induced cell apoptosis. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 8 Homo sapiens 49-52 24680927-8 2014 Taken together, the cell death of breast cancer cells in response to ziyuglycoside II was dependent upon cell cycle arrest and cell apoptosis via a ROS-dependent JNK activation pathway. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Homo sapiens 162-165 24576507-0 2014 HCC cells with high levels of Bcl-2 are resistant to ABT-737 via activation of the ROS-JNK-autophagy pathway. Reactive Oxygen Species 83-86 mitogen-activated protein kinase 8 Homo sapiens 87-90 24576507-5 2014 Moreover, autophagy suppressed the overactivation of the ROS-JNK pathway and protected against apoptosis. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 8 Homo sapiens 61-64 24576507-7 2014 In sum, this study indicated that the activation of the ROS-JNK-autophagy pathway may be an important mechanism by which HCC cells with high levels of Bcl-2 are resistant to ABT-737. Reactive Oxygen Species 56-59 mitogen-activated protein kinase 8 Homo sapiens 60-63 24692721-0 2014 Potent reactive oxygen species-JNK-p38 activation by sodium salicylate potentiates death of primary effusion lymphoma cells. Reactive Oxygen Species 7-30 mitogen-activated protein kinase 8 Homo sapiens 31-34 24582688-5 2014 Second, H2O2, the most important form of ROS in the cells in response to extracellular stress signals, can induce phosphorylation of the EZH2 protein and the activation of JNK, STAT3, and Akt. Reactive Oxygen Species 41-44 mitogen-activated protein kinase 8 Homo sapiens 172-175 23640957-8 2014 Overall, these findings for the first time suggest that ROS-mediated activation of cancer metabolism-related genes such as AMPK and JNK plays an important role in beta-sitosterol-induced apoptosis in U266 multiple myeloma cells. Reactive Oxygen Species 56-59 mitogen-activated protein kinase 8 Homo sapiens 132-135 24413150-0 2014 ROS-dependent activation of JNK converts p53 into an efficient inhibitor of oncogenes leading to robust apoptosis. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 28-31 24413150-5 2014 ROS promote the activation of c-Jun N-terminal kinase (JNK) and DNA damage response, which establishes a positive feedback loop with p53. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 30-53 24413150-5 2014 ROS promote the activation of c-Jun N-terminal kinase (JNK) and DNA damage response, which establishes a positive feedback loop with p53. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 55-58 24402682-0 2014 ROS-mediated JNK/p38-MAPK activation regulates Bax translocation in Sorafenib-induced apoptosis of EBV-transformed B cells. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 13-16 23640957-0 2014 Reactive oxygen species-mediated activation of AMP-activated protein kinase and c-Jun N-terminal kinase plays a critical role in beta-sitosterol-induced apoptosis in multiple myeloma U266 cells. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 80-103 23640957-2 2014 Thus, in the present study, the role of reactive oxygen species (ROS) in association with AMP-activated protein kinase (AMPK) and c-Jun N-terminal kinase (JNK) pathways was demonstrated in beta-sitosterol-treated multiple myeloma U266 cells. Reactive Oxygen Species 40-63 mitogen-activated protein kinase 8 Homo sapiens 130-153 23640957-2 2014 Thus, in the present study, the role of reactive oxygen species (ROS) in association with AMP-activated protein kinase (AMPK) and c-Jun N-terminal kinase (JNK) pathways was demonstrated in beta-sitosterol-treated multiple myeloma U266 cells. Reactive Oxygen Species 40-63 mitogen-activated protein kinase 8 Homo sapiens 155-158 23640957-2 2014 Thus, in the present study, the role of reactive oxygen species (ROS) in association with AMP-activated protein kinase (AMPK) and c-Jun N-terminal kinase (JNK) pathways was demonstrated in beta-sitosterol-treated multiple myeloma U266 cells. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 8 Homo sapiens 130-153 23640957-2 2014 Thus, in the present study, the role of reactive oxygen species (ROS) in association with AMP-activated protein kinase (AMPK) and c-Jun N-terminal kinase (JNK) pathways was demonstrated in beta-sitosterol-treated multiple myeloma U266 cells. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 8 Homo sapiens 155-158 23640957-7 2014 Furthermore, ROS scavenger N-acetyl L-cysteine attenuated beta-sitosterol-mediated sub-G1 accumulation, PARP cleavage, JNK and AMPK activation in U266 cells. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 119-122 24438216-10 2014 JNK activation was found to primarily depend on reactive oxygen species (ROS) resulting from the DHA treatment. Reactive Oxygen Species 48-71 mitogen-activated protein kinase 8 Homo sapiens 0-3 24374359-4 2014 The ROS elevation and ASK1 activation induced a sustained phosphorylation of c-Jun N-terminal kinase (JNK), while SP600125, as known as JNK inhibitor, almost reversed LW-214-induced apoptosis in MCF-7 cells. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 77-100 24374359-4 2014 The ROS elevation and ASK1 activation induced a sustained phosphorylation of c-Jun N-terminal kinase (JNK), while SP600125, as known as JNK inhibitor, almost reversed LW-214-induced apoptosis in MCF-7 cells. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 102-105 24438216-10 2014 JNK activation was found to primarily depend on reactive oxygen species (ROS) resulting from the DHA treatment. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Homo sapiens 0-3 24476312-0 2014 ent-kaurane diterpenoids from Croton tonkinensis induce apoptosis in colorectal cancer cells through the phosphorylation of JNK mediated by reactive oxygen species and dual-specificity JNK kinase MKK4. Reactive Oxygen Species 140-163 mitogen-activated protein kinase 8 Homo sapiens 124-127 24407242-6 2014 In conclusion, ER stress triggers an interaction of JNK with mitochondrial Sab, which leads to impaired respiration and increased mitochondrial reactive oxygen species, sustaining JNK activation culminating in apoptosis. Reactive Oxygen Species 144-167 mitogen-activated protein kinase 8 Homo sapiens 52-55 24407242-6 2014 In conclusion, ER stress triggers an interaction of JNK with mitochondrial Sab, which leads to impaired respiration and increased mitochondrial reactive oxygen species, sustaining JNK activation culminating in apoptosis. Reactive Oxygen Species 144-167 mitogen-activated protein kinase 8 Homo sapiens 180-183 24052408-3 2014 Here we report that two ROS generating phytochemicals, hydroxychavicol and curcumin synergize in leukemic cells in inducing enhanced apoptosis by independently activating both mitogen activated protein kinase (MAPK) (JNK and P(38)) and mTOR pathways. Reactive Oxygen Species 24-27 mitogen-activated protein kinase 8 Homo sapiens 217-220 24476312-8 2014 These findings suggest that ROS stimulated the phosphorylation of JNK mediated by MKK4 and played a critical role in CeKD-induced apoptosis in colorectal cancer cells. Reactive Oxygen Species 28-31 mitogen-activated protein kinase 8 Homo sapiens 66-69 24738081-6 2014 LQ-mediated cell viability reduction, mitochondrial dysfunction, apoptosis related protein abnormal expressions, and JNK and P38 activation were partially abolished by N-Acetyl-L-cysteine (a ROS inhibitor) pretreatment. Reactive Oxygen Species 191-194 mitogen-activated protein kinase 8 Homo sapiens 117-120 24967005-0 2014 Piperlongumine inhibits migration of glioblastoma cells via activation of ROS-dependent p38 and JNK signaling pathways. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 96-99 25502879-14 2014 Furthermore, mPTP opening was directly regulated by ROS/JNK pathway. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Homo sapiens 56-59 24211866-0 2014 The activation of p38 and JNK by ROS, contribute to OLO-2-mediated intrinsic apoptosis in human hepatocellular carcinoma cells. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 26-29 24357804-0 2013 The ROS/JNK/ATF2 pathway mediates selenite-induced leukemia NB4 cell cycle arrest and apoptosis in vitro and in vivo. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 8-11 25462060-2 2014 Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 112-115 mitogen-activated protein kinase 8 Homo sapiens 230-253 25462060-2 2014 Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 112-115 mitogen-activated protein kinase 8 Homo sapiens 255-258 24357804-4 2013 Further experiments demonstrated that selenite-induced production of reactive oxygen species (ROS) worked as an upstream of the JNK/ATF2 axis, cell cycle arrest and apoptosis. Reactive Oxygen Species 69-92 mitogen-activated protein kinase 8 Homo sapiens 128-131 24357804-4 2013 Further experiments demonstrated that selenite-induced production of reactive oxygen species (ROS) worked as an upstream of the JNK/ATF2 axis, cell cycle arrest and apoptosis. Reactive Oxygen Species 94-97 mitogen-activated protein kinase 8 Homo sapiens 128-131 24357804-7 2013 Taken together, our results indicate that selenite-induced ROS arrest NB4 cells at G0/G1 phase through inhibiting the JNK/ATF2 axis in vitro and in vivo. Reactive Oxygen Species 59-62 mitogen-activated protein kinase 8 Homo sapiens 118-121 24025361-10 2013 BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3. Reactive Oxygen Species 34-57 mitogen-activated protein kinase 8 Homo sapiens 142-145 24115572-4 2013 We show that p38 MAPK inhibition results in ROS upregulation, which in turn activates the JNK pathway via inactivation of phosphatases, sensitizing human tumour cells to cisplatin-induced apoptosis. Reactive Oxygen Species 44-47 mitogen-activated protein kinase 8 Homo sapiens 90-93 24025361-10 2013 BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3. Reactive Oxygen Species 59-62 mitogen-activated protein kinase 8 Homo sapiens 142-145 24025361-10 2013 BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 142-145 24008433-9 2013 In addition, the ROS scavenger melatonin almost completely blocked Phx-3-induced JNK activation and apoptosis. Reactive Oxygen Species 17-20 mitogen-activated protein kinase 8 Homo sapiens 81-84 24008433-10 2013 This suggests that JNK activation was mediated by Phx-3-induced ROS generation. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 19-22 24008433-13 2013 These results indicate that the production of ROS following JNK activation is the main axis of Phx-3-induced apoptosis in LN229 cells for short-term exposure to Phx-3, whereas alternative mechanism(s) appear to be involved in apoptosis induction during long-term exposure to Phx-3. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 60-63 24176849-7 2013 ROS generation caused depletion of thiol groups and glutathione, activation of c-Jun N-terminal kinase (JNK) and downregulation of nuclear factor kB (NF-kB). Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 104-107 24040019-0 2013 Synergistic apoptosis of CML cells by buthionine sulfoximine and hydroxychavicol correlates with activation of AIF and GSH-ROS-JNK-ERK-iNOS pathway. Reactive Oxygen Species 123-126 mitogen-activated protein kinase 8 Homo sapiens 127-130 24158003-8 2013 Collectively, combination treatment with bortezomib and 2ME induces cell death via JNK-MKK4/7 activation by overproduction of mitochondrial ROS. Reactive Oxygen Species 140-143 mitogen-activated protein kinase 8 Homo sapiens 83-86 24086554-7 2013 Taken together, our data suggest that XO mediates LPS-induced phosphorylation of JNK through ROS production and MKP-1 inactivation, leading to MCP-1 production in macrophages. Reactive Oxygen Species 93-96 mitogen-activated protein kinase 8 Homo sapiens 81-84 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 8 Homo sapiens 29-32 24040019-13 2013 CONCLUSION/SIGNIFICANCE: BSO synergizes with HCH in inducing apoptosis of CML cells through the GSH-ROS-JNK-ERK-iNOS pathway. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 8 Homo sapiens 104-107 23633517-8 2013 The ROS-reducing enzyme catalase is destabilized in an ERK- and JNK-dependent manner in RIP1 knockdown HBECs and application of catalase effectively blocked BPDE-induced ROS accumulation and cytotoxicity. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 64-67 23728448-3 2013 Persistent c-Jun N-terminal kinase (JNK) activity in VS cells reduces cell death by suppressing the accumulation of reactive oxygen species (ROS), raising the possibility that JNK activity protects against IR-induced VS cell death, which is mediated by ROS. Reactive Oxygen Species 116-139 mitogen-activated protein kinase 8 Homo sapiens 11-34 23824739-4 2013 We found that simultaneous inhibition of TXNRD1 and AKT pathways induced robust reactive oxygen species production, which was involved in c-jun-NH2-kinase (JNK; MAPK8) activation and cell apoptosis. Reactive Oxygen Species 80-103 mitogen-activated protein kinase 8 Homo sapiens 138-154 23824739-4 2013 We found that simultaneous inhibition of TXNRD1 and AKT pathways induced robust reactive oxygen species production, which was involved in c-jun-NH2-kinase (JNK; MAPK8) activation and cell apoptosis. Reactive Oxygen Species 80-103 mitogen-activated protein kinase 8 Homo sapiens 156-159 23824739-4 2013 We found that simultaneous inhibition of TXNRD1 and AKT pathways induced robust reactive oxygen species production, which was involved in c-jun-NH2-kinase (JNK; MAPK8) activation and cell apoptosis. Reactive Oxygen Species 80-103 mitogen-activated protein kinase 8 Homo sapiens 161-166 23728448-3 2013 Persistent c-Jun N-terminal kinase (JNK) activity in VS cells reduces cell death by suppressing the accumulation of reactive oxygen species (ROS), raising the possibility that JNK activity protects against IR-induced VS cell death, which is mediated by ROS. Reactive Oxygen Species 141-144 mitogen-activated protein kinase 8 Homo sapiens 11-34 23728448-3 2013 Persistent c-Jun N-terminal kinase (JNK) activity in VS cells reduces cell death by suppressing the accumulation of reactive oxygen species (ROS), raising the possibility that JNK activity protects against IR-induced VS cell death, which is mediated by ROS. Reactive Oxygen Species 141-144 mitogen-activated protein kinase 8 Homo sapiens 36-39 23728448-3 2013 Persistent c-Jun N-terminal kinase (JNK) activity in VS cells reduces cell death by suppressing the accumulation of reactive oxygen species (ROS), raising the possibility that JNK activity protects against IR-induced VS cell death, which is mediated by ROS. Reactive Oxygen Species 253-256 mitogen-activated protein kinase 8 Homo sapiens 11-34 23728448-3 2013 Persistent c-Jun N-terminal kinase (JNK) activity in VS cells reduces cell death by suppressing the accumulation of reactive oxygen species (ROS), raising the possibility that JNK activity protects against IR-induced VS cell death, which is mediated by ROS. Reactive Oxygen Species 116-139 mitogen-activated protein kinase 8 Homo sapiens 36-39 23728448-3 2013 Persistent c-Jun N-terminal kinase (JNK) activity in VS cells reduces cell death by suppressing the accumulation of reactive oxygen species (ROS), raising the possibility that JNK activity protects against IR-induced VS cell death, which is mediated by ROS. Reactive Oxygen Species 253-256 mitogen-activated protein kinase 8 Homo sapiens 36-39 23728448-3 2013 Persistent c-Jun N-terminal kinase (JNK) activity in VS cells reduces cell death by suppressing the accumulation of reactive oxygen species (ROS), raising the possibility that JNK activity protects against IR-induced VS cell death, which is mediated by ROS. Reactive Oxygen Species 253-256 mitogen-activated protein kinase 8 Homo sapiens 176-179 23812630-8 2013 Conclusively, our results suggested that apoptosis in response to olaquindox treatment in HepG2 cells might be suppressed through p38 MAPK and ROS-JNK pathways. Reactive Oxygen Species 143-146 mitogen-activated protein kinase 8 Homo sapiens 147-150 23728448-13 2013 CONCLUSION: Inhibition of JNK signaling decreases histone 2AX phosphorylation and increases ROS and apoptosis in VS cells after gamma irradiation. Reactive Oxygen Species 92-95 mitogen-activated protein kinase 8 Homo sapiens 26-29 23812630-0 2013 Olaquindox-induced apoptosis is suppressed through p38 MAPK and ROS-mediated JNK pathways in HepG2 cells. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 77-80 23812630-6 2013 In addition, the levels of phosphorylation of JNK, but not p38 MAPK, were significantly suppressed after pretreatment of the antioxidants, while inhibition of the activations of JNK or p38 MAPK had no effect on ROS generation. Reactive Oxygen Species 211-214 mitogen-activated protein kinase 8 Homo sapiens 46-49 23812630-7 2013 This result suggested that ROS may be the upstream mediator for the activation of JNK. Reactive Oxygen Species 27-30 mitogen-activated protein kinase 8 Homo sapiens 82-85 23760395-11 2013 Moreover, we observed that MQ-mediated ROS simultaneously downregulated Akt phosphorylation and activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and adenosine monophosphate-activated protein kinase (AMPK) signaling in PC3 cells. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 8 Homo sapiens 151-174 23708648-10 2013 Furthermore, the khat-induced reactive oxygen species (ROS) production and the activation of the ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the khat-induced activation of JNK and ERK. Reactive Oxygen Species 30-53 mitogen-activated protein kinase 8 Homo sapiens 181-184 23708648-10 2013 Furthermore, the khat-induced reactive oxygen species (ROS) production and the activation of the ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the khat-induced activation of JNK and ERK. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 8 Homo sapiens 181-184 23708648-10 2013 Furthermore, the khat-induced reactive oxygen species (ROS) production and the activation of the ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the khat-induced activation of JNK and ERK. Reactive Oxygen Species 97-100 mitogen-activated protein kinase 8 Homo sapiens 181-184 23417568-7 2013 Thus, we declare that ROS type has a key role in selective instigation of JNK/p38-MAPKs and JAK2-STAT3 pathways in SK-N-MC cells. Reactive Oxygen Species 22-25 mitogen-activated protein kinase 8 Homo sapiens 74-77 23607503-4 2013 H2O2-induced ROS increased the phosphorylation of p38 MAPK and JNK; this was inhibited by DK pretreatment. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 63-66 23530055-6 2013 Our data suggest that IKK has a dual role: a transcription-dependent and a transcription-independent action in controlling the ASK1-JNK axis, coupling IKK to ROS and ER stress response. Reactive Oxygen Species 158-161 mitogen-activated protein kinase 8 Homo sapiens 132-135 23760395-0 2013 Mefloquine exerts anticancer activity in prostate cancer cells via ROS-mediated modulation of Akt, ERK, JNK and AMPK signaling. Reactive Oxygen Species 67-70 mitogen-activated protein kinase 8 Homo sapiens 104-107 23760395-11 2013 Moreover, we observed that MQ-mediated ROS simultaneously downregulated Akt phosphorylation and activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and adenosine monophosphate-activated protein kinase (AMPK) signaling in PC3 cells. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 8 Homo sapiens 176-179 23376438-7 2013 Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability. Reactive Oxygen Species 158-181 mitogen-activated protein kinase 8 Homo sapiens 32-55 23376438-7 2013 Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability. Reactive Oxygen Species 158-181 mitogen-activated protein kinase 8 Homo sapiens 57-60 23376438-10 2013 Collectively, these results suggest that the activation of p53, JNK or p38 kinase by ZEN metabolites is the main upstream signal required for the mitochondrial alteration of Bcl-2/Bax signaling pathways and intracellular ROS generation, while MMP loss and nuclear translocation of AIF are the critical downstream events for ZEN metabolite-mediated apoptosis in macrophages. Reactive Oxygen Species 221-224 mitogen-activated protein kinase 8 Homo sapiens 64-67 23376438-7 2013 Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability. Reactive Oxygen Species 183-186 mitogen-activated protein kinase 8 Homo sapiens 32-55 23376438-7 2013 Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability. Reactive Oxygen Species 183-186 mitogen-activated protein kinase 8 Homo sapiens 57-60 23394457-12 2013 In addition, JNK signaling pathway was activated by hirsutanol A through elevating ROS level. Reactive Oxygen Species 83-86 mitogen-activated protein kinase 8 Homo sapiens 13-16 23394457-13 2013 Blockade of JNK signaling pathway by JNK specific inhibitor SP600125 enhanced apoptosis and hirsutanol A-induced ROS accumulation. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 8 Homo sapiens 12-15 23394457-13 2013 Blockade of JNK signaling pathway by JNK specific inhibitor SP600125 enhanced apoptosis and hirsutanol A-induced ROS accumulation. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 8 Homo sapiens 37-40 23222262-12 2013 CONCLUSIONS: Interleukin-8 induction by wood smoke extract in lung epithelial cells is mediated by novel NADPH oxidase-dependent, reactive oxygen species-sensitive AMP-activated protein kinase signaling with Jun N-terminal kinase and extracellular signal-regulated kinase as the downstream kinases and nuclear factor-kappaB and signal transducer and activator of transcription protein 3 as the downstream transcription factors. Reactive Oxygen Species 130-153 mitogen-activated protein kinase 8 Homo sapiens 208-229 23222262-7 2013 Removal of intracellular reactive oxygen species by N-acetyl-cysteine reduced the activation of AMP-activated protein kinase, extracellular signal-regulated kinase and Jun N-terminal kinase, and interleukin-8 induction. Reactive Oxygen Species 25-48 mitogen-activated protein kinase 8 Homo sapiens 168-189 23063000-3 2013 There is now compelling evidences that the NF-kappaB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). Reactive Oxygen Species 119-142 mitogen-activated protein kinase 8 Homo sapiens 57-60 23063000-3 2013 There is now compelling evidences that the NF-kappaB and JNK pathways are activated by cytokines induced generation of reactive oxygen species (ROS). Reactive Oxygen Species 144-147 mitogen-activated protein kinase 8 Homo sapiens 57-60 23063000-7 2013 In addition, most of the genes, known to be inducible by NF-kappaB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. Reactive Oxygen Species 237-240 mitogen-activated protein kinase 8 Homo sapiens 70-73 22707385-8 2012 Downstream production of ROS may derive from mitochondria damage and secondary injuries, possibly determining the second cycle of GRP78, IRE-1alpha, caspase-2 and JNK activation. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Homo sapiens 163-166 23041154-5 2012 Reactive oxygen species, as the major players in oxidative stress, guide FOXO1 nuclear localization at least by simultaneous c-Jun N-terminal kinase (JNK) activation and Akt/PKB activity suppression. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 125-148 23041154-5 2012 Reactive oxygen species, as the major players in oxidative stress, guide FOXO1 nuclear localization at least by simultaneous c-Jun N-terminal kinase (JNK) activation and Akt/PKB activity suppression. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 150-153 22922338-0 2012 Capsazepine, a TRPV1 antagonist, sensitizes colorectal cancer cells to apoptosis by TRAIL through ROS-JNK-CHOP-mediated upregulation of death receptors. Reactive Oxygen Species 98-101 mitogen-activated protein kinase 8 Homo sapiens 102-105 22354145-0 2012 AW00179 potentiates TRAIL-mediated death of human lung cancer H1299 cells through ROS-JNK-c-Jun-mediated up-regulation of DR5 and down-regulation of anti-apoptotic molecules. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 86-89 22922338-9 2012 Furthermore, ROS sequestration abrogated the activation of JNK. Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 59-62 22922338-11 2012 Together, our results indicate that capsazepine potentiates the apoptotic effects of TRAIL through downregulation of cell survival proteins and upregulation of death receptors via the ROS-JNK-CHOP-mediated pathway. Reactive Oxygen Species 184-187 mitogen-activated protein kinase 8 Homo sapiens 188-191 22981381-0 2012 Diallyl trisulfide induces apoptosis in human breast cancer cells through ROS-mediated activation of JNK and AP-1. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 101-104 23047827-0 2012 Triglyceride accumulation in macrophages upregulates paraoxonase 2 (PON2) expression via ROS-mediated JNK/c-Jun signaling pathway activation. Reactive Oxygen Species 89-92 mitogen-activated protein kinase 8 Homo sapiens 102-105 22354145-7 2012 In conclusion, AW00179 has the potential to sensitize H1299 cells to TRAIL-mediated apoptosis through two distinct mechanisms: ROS-JNK-c-Jun-mediated up-regulation of DR5, and down-regulation of anti-apoptotic molecules. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 131-134 22946656-7 2012 Moreover, ar-turmerone stimulated c-Jun N-terminal kinase (JNK) and extracellular signal-related kinase (ERK) phosphorylation and activation; treatment with JNK and ERK inhibitors markedly reduced PUMA, Bax, Fas, and DR4 levels and reduced apoptosis but not ROS generation. Reactive Oxygen Species 258-261 mitogen-activated protein kinase 8 Homo sapiens 157-160 22906494-11 2012 The data suggest that the mechanism of menadione-induced JNK activation involves the production of reactive oxygen species, likely superoxide anion, and intracellular GSH levels play an important role in preventing GSTA1-JNK complex dissociation, subsequent JNK activation and induction of cytotoxicity. Reactive Oxygen Species 99-122 mitogen-activated protein kinase 8 Homo sapiens 57-60 22946656-9 2012 Taken together, these results suggest that ar-turmerone-induced apoptosis in HepG2 cells is through ROS-mediated activation of ERK and JNK kinases and triggers both intrinsic and extrinsic caspase activation, leading to apoptosis. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 8 Homo sapiens 135-138 22771329-0 2012 Reactive oxygen species-mediated activation of JNK and down-regulation of DAXX are critically involved in penta-O-galloyl-beta-d-glucose-induced apoptosis in chronic myeloid leukemia K562 cells. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 47-50 22607092-10 2012 JNK and p53 have been shown to mediate the depletion of GSH [ 2 , 3 ], and we previously demonstrated the existence of a ROS-JNK-p53 cycle in silibinin-treated HeLa cells [ 4 ]. Reactive Oxygen Species 121-124 mitogen-activated protein kinase 8 Homo sapiens 125-128 22668848-6 2012 Knockdown of JNK by siRNA efficiently inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by BBP, indicating that JNK activation may be a upstream signaling of ROS and should be a core component in BBP-induced autophagic signaling pathway. Reactive Oxygen Species 48-51 mitogen-activated protein kinase 8 Homo sapiens 13-16 22668848-6 2012 Knockdown of JNK by siRNA efficiently inhibited ROS production and autophagy, but antioxidant NAC failed to block JNK activation induced by BBP, indicating that JNK activation may be a upstream signaling of ROS and should be a core component in BBP-induced autophagic signaling pathway. Reactive Oxygen Species 207-210 mitogen-activated protein kinase 8 Homo sapiens 13-16 22668848-7 2012 These results suggest that BBP produces its growth inhibitory effect through induction of the autophagic cell death in MCF-7 cells, which is modulated by a JNK-dependent Atg4 upregulation involving ROS production. Reactive Oxygen Species 198-201 mitogen-activated protein kinase 8 Homo sapiens 156-159 22771329-7 2012 Of note, ROS inhibitor acetyl-L-cysteine (NAC) reversed JNK-dependent apoptosis and DAXX inhibition induced by PGG. Reactive Oxygen Species 9-12 mitogen-activated protein kinase 8 Homo sapiens 56-59 22771329-8 2012 Overall, these findings suggest that ROS-dependent JNK activation and DAXX downregulation are critically involved in PGG-induced apoptosis in K562 cells. Reactive Oxygen Species 37-40 mitogen-activated protein kinase 8 Homo sapiens 51-54 22575822-7 2012 These results suggest that Cheongja 3 black soybean seed coat anthocyanins have brain neuroprotective effects against oxidative stress (H(2)O(2)) by inhibiting the activation of ASK1-JNK/p38 pathways, scavenging ROS, stimulating the expression of HO-1 and, more interestingly, recruiting cellular free sialic acids through up-regulation of Neu1 sialidase gene expression. Reactive Oxygen Species 212-215 mitogen-activated protein kinase 8 Homo sapiens 183-186 22687635-7 2012 In addition, the apoptotic effect of Baohuoside I was dependent on the activation of ROS downstream effectors, JNK and p38(MAPK), which could be almost abrogated by using inhibitors SB203580 (an inhibitor of p38(MAPK)) and SP600125 (an inhibitor of JNK). Reactive Oxygen Species 85-88 mitogen-activated protein kinase 8 Homo sapiens 111-114 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 8 Homo sapiens 139-142 22681760-9 2012 Snake venom toxin also induced JNK phosphorylation and ROS generation, however, pretreatment of JNK inhibitor and ROS scavenger reversed the inhibitory effect of snake venom toxin on cancer cell proliferation, and reduced the snake venom toxin-induced upregulation of DR4 and DR5 expression. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 8 Homo sapiens 96-99 22681760-9 2012 Snake venom toxin also induced JNK phosphorylation and ROS generation, however, pretreatment of JNK inhibitor and ROS scavenger reversed the inhibitory effect of snake venom toxin on cancer cell proliferation, and reduced the snake venom toxin-induced upregulation of DR4 and DR5 expression. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Homo sapiens 31-34 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 8 Homo sapiens 225-228 22252531-0 2012 ICB3E induces iNOS expression by ROS-dependent JNK and ERK activation for apoptosis of leukemic cells. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 47-50 22252531-6 2012 Unlike HCH, ICB3E treatment caused ROS dependent activation of both JNK, ERK and induced the expression of iNOS leading to generation of nitric oxide (NO). Reactive Oxygen Species 35-38 mitogen-activated protein kinase 8 Homo sapiens 68-71 22252531-9 2012 Our data reveal a novel ROS-dependent JNK/ERK-mediated iNOS activation pathway which leads to NO mediated cell death by ICB3E. Reactive Oxygen Species 24-27 mitogen-activated protein kinase 8 Homo sapiens 38-41 22427461-0 2012 Induction of apoptosis by casticin in cervical cancer cells: reactive oxygen species-dependent sustained activation of Jun N-terminal kinase. Reactive Oxygen Species 61-84 mitogen-activated protein kinase 8 Homo sapiens 119-140 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 8 Homo sapiens 225-228 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 8 Homo sapiens 62-65 22293863-6 2012 The MEK inhibitor decreased O2 - levels in ATO-treated HPF cells whereas JNK and p38 inhibitors generally increased ROS levels including O2 - in these cells. Reactive Oxygen Species 128-131 mitogen-activated protein kinase 8 Homo sapiens 85-88 21074392-6 2012 Attenuation of JNK expression in the presence of NAC might indicate the modulation of the level of JNK activity by ROS. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 8 Homo sapiens 15-18 21074392-6 2012 Attenuation of JNK expression in the presence of NAC might indicate the modulation of the level of JNK activity by ROS. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 8 Homo sapiens 99-102 22293863-9 2012 In addition, JNK and p38 siRNAs increased ROS levels and GSH depletion in ATO-treated HPF cells. Reactive Oxygen Species 54-57 mitogen-activated protein kinase 8 Homo sapiens 13-16 22293863-11 2012 siRNAs targeting JNK and p38 showing an increase in ROS levels and GSH depletion in ATO-treated HPF cells augmented cell growth inhibition and death. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 17-20 22540380-8 2012 CONCLUSIONS: Our data suggest that Cas III-ia induces cell death by autophagy and apoptosis, in part due to the activation of ROS -dependent JNK signaling. Reactive Oxygen Species 126-129 mitogen-activated protein kinase 8 Homo sapiens 141-144 22245672-10 2012 Taken together, these findings suggest that human IM is able to metabolize GS into GP, and the related biological activities induce apoptosis through ROS/JNK signaling. Reactive Oxygen Species 150-153 mitogen-activated protein kinase 8 Homo sapiens 154-157 22064324-11 2012 The present study delineates that BMP4 causes EC apoptosis through activation of caspase-3 in a ROS/p38MAPK/JNK-dependent signaling cascade. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 8 Homo sapiens 108-111 22321643-4 2012 ROS mediated c-Jun NH(2)-terminal kinase (JNK) is also required for AP-1 activation, but Syk and PI3K regulated AP-1 activation independently of JNK. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 13-40 22321643-4 2012 ROS mediated c-Jun NH(2)-terminal kinase (JNK) is also required for AP-1 activation, but Syk and PI3K regulated AP-1 activation independently of JNK. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 42-45 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 8 Homo sapiens 130-133 22002081-7 2012 Inhibition of ROS generation abolished AMPK activation by AICAR as well as JNK and caspase-3 activation. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 87-90 22863969-7 2012 The fomitoside-K induced cell death by ROS was significantly inhibited by NAC, ERK (PD98059) and JNK inhibitor (SP600125). Reactive Oxygen Species 39-42 mitogen-activated protein kinase 8 Homo sapiens 97-100 21625221-0 2011 NF-kappaB suppresses ROS levels in BCR-ABL(+) cells to prevent activation of JNK and cell death. Reactive Oxygen Species 21-24 mitogen-activated protein kinase 8 Homo sapiens 77-80 23028492-7 2012 Salinomycin also led to the formation of reactive oxygen species (ROS) eliciting JNK activation and induction of the transcription factor JUN. Reactive Oxygen Species 41-64 mitogen-activated protein kinase 8 Homo sapiens 81-84 23028492-7 2012 Salinomycin also led to the formation of reactive oxygen species (ROS) eliciting JNK activation and induction of the transcription factor JUN. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Homo sapiens 81-84 21771752-16 2011 HHE-mediated accumulation of ROS may induce redox-sensitive transcription factor, NF-kappaB, through activation of ERK and JNK, resulting in cellular apoptosis in HK-2 cells. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 8 Homo sapiens 123-126 21763418-7 2011 ROS activated autophagy via the c-Jun NH(2)-terminal kinase (JNK). Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 32-59 21911753-9 2011 CONCLUSIONS: We provide the first in vitro and in vivo evidence in support of an accelerated Rac1-Nox-ROS-JNK1/2 signaling pathway in the islet beta-cell leading to the onset of mitochondrial dysregulation in diabetes. Reactive Oxygen Species 102-105 mitogen-activated protein kinase 8 Homo sapiens 106-110 21763418-7 2011 ROS activated autophagy via the c-Jun NH(2)-terminal kinase (JNK). Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 61-64 21618589-6 2011 Doxorubicin also augmented DNA fragmentation and increased the phosphorylation of ROS-sensitive pro-apoptotic kinase c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 117-140 21676946-0 2011 The SUMO E3-ligase PIAS1 couples reactive oxygen species-dependent JNK activation to oxidative cell death. Reactive Oxygen Species 33-56 mitogen-activated protein kinase 8 Homo sapiens 67-70 21676946-1 2011 Human endometrial stromal cells (HESCs) exposed to reactive oxygen species (ROS) mount a hypersumoylation response in a c-Jun N-terminal kinase (JNK)-dependent manner. Reactive Oxygen Species 51-74 mitogen-activated protein kinase 8 Homo sapiens 120-143 21676946-1 2011 Human endometrial stromal cells (HESCs) exposed to reactive oxygen species (ROS) mount a hypersumoylation response in a c-Jun N-terminal kinase (JNK)-dependent manner. Reactive Oxygen Species 51-74 mitogen-activated protein kinase 8 Homo sapiens 145-148 21676946-1 2011 Human endometrial stromal cells (HESCs) exposed to reactive oxygen species (ROS) mount a hypersumoylation response in a c-Jun N-terminal kinase (JNK)-dependent manner. Reactive Oxygen Species 76-79 mitogen-activated protein kinase 8 Homo sapiens 120-143 21676946-1 2011 Human endometrial stromal cells (HESCs) exposed to reactive oxygen species (ROS) mount a hypersumoylation response in a c-Jun N-terminal kinase (JNK)-dependent manner. Reactive Oxygen Species 76-79 mitogen-activated protein kinase 8 Homo sapiens 145-148 21676946-3 2011 We show that ROS-dependent JNK activation converges on the SUMO pathway via PIAS1 (protein inhibitor of activated STAT1). Reactive Oxygen Species 13-16 mitogen-activated protein kinase 8 Homo sapiens 27-30 21676946-5 2011 Conversely, PIAS overexpression increased sumoylation of various substrates, including c-Jun, yet inhibited basal and ROS-dependent JNK activity independently of its SUMO ligase function. Reactive Oxygen Species 118-121 mitogen-activated protein kinase 8 Homo sapiens 132-135 21618589-6 2011 Doxorubicin also augmented DNA fragmentation and increased the phosphorylation of ROS-sensitive pro-apoptotic kinase c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 142-145 21761924-12 2011 Altogether, these experiments suggest that ROS formation may play an important role in the genotoxicity of magnetite in A549 cells but that activation of JNK seems to be ROS-independent. Reactive Oxygen Species 170-173 mitogen-activated protein kinase 8 Homo sapiens 154-157 21697181-8 2011 Furthermore, ebselen, a ROS scavenger, rescued VS cells with suppressed JNK from apoptosis, suggesting that JNK activity protects VS cells from apoptosis by limiting accumulation of ROS. Reactive Oxygen Species 182-185 mitogen-activated protein kinase 8 Homo sapiens 108-111 21050133-13 2011 We conclude that HGF-induced mobilization of EPCs and the proangiogenic effects of the growth factor require a Nox2-dependent ROS-mediated activation of Jak2 and Jnk. Reactive Oxygen Species 126-129 mitogen-activated protein kinase 8 Homo sapiens 162-165 21697181-7 2011 Inhibition of JNK increased the fluorescence intensity of VS cells loaded with 5-(and-6)-chloromethyl-2",7"-dichlorodihydrofluorescein diacetate (H(2)DCFDA), a fluorescent probe for reactive oxygen species (ROS). Reactive Oxygen Species 182-205 mitogen-activated protein kinase 8 Homo sapiens 14-17 21697181-7 2011 Inhibition of JNK increased the fluorescence intensity of VS cells loaded with 5-(and-6)-chloromethyl-2",7"-dichlorodihydrofluorescein diacetate (H(2)DCFDA), a fluorescent probe for reactive oxygen species (ROS). Reactive Oxygen Species 207-210 mitogen-activated protein kinase 8 Homo sapiens 14-17 21391979-10 2011 Generation of ROS induced phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK), p38 MAPK and JNK1/2, which was attenuated by DPI and APO and the ROS scavenger N-acetylcysteine. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 107-113 21391979-10 2011 Generation of ROS induced phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK), p38 MAPK and JNK1/2, which was attenuated by DPI and APO and the ROS scavenger N-acetylcysteine. Reactive Oxygen Species 159-162 mitogen-activated protein kinase 8 Homo sapiens 107-113 21454558-0 2011 Mitochondrial c-Jun N-terminal kinase (JNK) signaling initiates physiological changes resulting in amplification of reactive oxygen species generation. Reactive Oxygen Species 116-139 mitogen-activated protein kinase 8 Homo sapiens 14-37 24980815-1 2014 We have shown previously that Gugggulsterone (Gug) inhibits growth of cultured LNCaP and PC-3 human prostate cancer cells by causing apoptosis induction in association with reactive-oxygen species (ROS)-dependent activation of c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 173-196 mitogen-activated protein kinase 8 Homo sapiens 227-250 24980815-1 2014 We have shown previously that Gugggulsterone (Gug) inhibits growth of cultured LNCaP and PC-3 human prostate cancer cells by causing apoptosis induction in association with reactive-oxygen species (ROS)-dependent activation of c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 173-196 mitogen-activated protein kinase 8 Homo sapiens 252-255 24980815-1 2014 We have shown previously that Gugggulsterone (Gug) inhibits growth of cultured LNCaP and PC-3 human prostate cancer cells by causing apoptosis induction in association with reactive-oxygen species (ROS)-dependent activation of c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 198-201 mitogen-activated protein kinase 8 Homo sapiens 227-250 24980815-1 2014 We have shown previously that Gugggulsterone (Gug) inhibits growth of cultured LNCaP and PC-3 human prostate cancer cells by causing apoptosis induction in association with reactive-oxygen species (ROS)-dependent activation of c-Jun N-terminal kinase (JNK). Reactive Oxygen Species 198-201 mitogen-activated protein kinase 8 Homo sapiens 252-255 21569548-17 2011 JNK was activated by celastrol-induced ROS accumulation and then initiated mitochondrial-mediated apoptosis. Reactive Oxygen Species 39-42 mitogen-activated protein kinase 8 Homo sapiens 0-3 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 8 Homo sapiens 116-122 21559503-6 2011 Cytotoxicity of Fe-SP and activation of caspase-3, -7, PARP, pro-apoptotic p38 and JNK MAPK could be prevented by co-treatment with antioxidants suggesting ROS generation is the primary mechanism of cytotoxic action. Reactive Oxygen Species 156-159 mitogen-activated protein kinase 8 Homo sapiens 83-86 21300795-11 2011 Our results provide novel evidence that autophagy is critically involved in malignant transformation by oncogenic K-Ras and show that reactive oxygen species-mediated JNK activation plays a causal role in autophagy induction through up-regulation of ATG5 and ATG7. Reactive Oxygen Species 134-157 mitogen-activated protein kinase 8 Homo sapiens 167-170 21454558-0 2011 Mitochondrial c-Jun N-terminal kinase (JNK) signaling initiates physiological changes resulting in amplification of reactive oxygen species generation. Reactive Oxygen Species 116-139 mitogen-activated protein kinase 8 Homo sapiens 39-42 21454558-4 2011 We observed that inhibition of JNK activity and JNK silencing with siRNA reduced the level of reactive oxygen species (ROS) generated during anisomycin-induced stress in HeLa cells. Reactive Oxygen Species 94-117 mitogen-activated protein kinase 8 Homo sapiens 48-51 21454558-4 2011 We observed that inhibition of JNK activity and JNK silencing with siRNA reduced the level of reactive oxygen species (ROS) generated during anisomycin-induced stress in HeLa cells. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 8 Homo sapiens 48-51 21454558-6 2011 Moreover, JNK signaling mediated amplification of ROS production during stress. Reactive Oxygen Species 50-53 mitogen-activated protein kinase 8 Homo sapiens 10-13 21454558-7 2011 Mitochondrial superoxide production was shown to be the source of JNK-induced ROS amplification, as an NADPH oxidase inhibitor demonstrated little impact on JNK-mediated ROS generation. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 8 Homo sapiens 66-69 21454558-9 2011 These results suggest that cellular stress altered mitochondria, causing JNK to translocate to the mitochondria and amplify up to 80% of the ROS generated largely by Complex I. Reactive Oxygen Species 141-144 mitogen-activated protein kinase 8 Homo sapiens 73-76 21454558-10 2011 This work demonstrates that a sequence of events exist for JNK mitochondrial signaling whereby ROS activates JNK, thereby affecting mitochondrial physiology, which can have effects on cell survival and death. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 8 Homo sapiens 59-62 21454558-10 2011 This work demonstrates that a sequence of events exist for JNK mitochondrial signaling whereby ROS activates JNK, thereby affecting mitochondrial physiology, which can have effects on cell survival and death. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 8 Homo sapiens 109-112 21115635-11 2011 In conclusion, the present study indicates that ROS-dependent apoptosis by GL is regulated by JNK signaling axis. Reactive Oxygen Species 48-51 mitogen-activated protein kinase 8 Homo sapiens 94-97 21562587-7 2011 Furthermore, in cultured cells, CM caused a dose-response increase in reactive oxygen species (ROS) production, which triggered Jun N-terminal kinases (JNK1/2) and p38 stress kinases marked activation and thus apoptosis. Reactive Oxygen Species 70-93 mitogen-activated protein kinase 8 Homo sapiens 152-158 21562587-7 2011 Furthermore, in cultured cells, CM caused a dose-response increase in reactive oxygen species (ROS) production, which triggered Jun N-terminal kinases (JNK1/2) and p38 stress kinases marked activation and thus apoptosis. Reactive Oxygen Species 95-98 mitogen-activated protein kinase 8 Homo sapiens 152-158 21919841-6 2011 ROS can activate cell-death pathways such as the c-Jun Nterminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways, which in turn, induce hair cell apoptosis. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 49-71 21047991-12 2011 Additionally, ROS generated by Cr(VI) is a pivotal regulator of JNK. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 64-67 21166414-8 2011 In relation to ROS and GSH levels, JNK and p38 inhibitors increased ROS levels, and GSH-depleted cell numbers in GA-treated HeLa cells. Reactive Oxygen Species 15-18 mitogen-activated protein kinase 8 Homo sapiens 35-38 21166414-8 2011 In relation to ROS and GSH levels, JNK and p38 inhibitors increased ROS levels, and GSH-depleted cell numbers in GA-treated HeLa cells. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 35-38 21166414-11 2011 Conclusively, JNK and p38 inhibitors and p38 siRNA enhanced growth inhibition and cell death in GA-treated HeLa cells, which were to some extent related to GSH depletion and ROS levels, especially O(2)( -). Reactive Oxygen Species 174-177 mitogen-activated protein kinase 8 Homo sapiens 14-17 21919841-6 2011 ROS can activate cell-death pathways such as the c-Jun Nterminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways, which in turn, induce hair cell apoptosis. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 73-76 21078900-9 2010 Inhibition of ROS generation completely blocked phosphorylation of JNK and p38 MAPK and induction of ER stress-related genes. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 67-70 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 8 Homo sapiens 180-183 19861509-0 2011 Agaricus blazei Extract Induces Apoptosis through ROS-Dependent JNK Activation Involving the Mitochondrial Pathway and Suppression of Constitutive NF-kappaB in THP-1 Cells. Reactive Oxygen Species 50-53 mitogen-activated protein kinase 8 Homo sapiens 64-67 19861509-7 2011 We concluded that ABE induces apoptosis with ROS-dependent JNK activation and constitutive activated NF-kappaB inhibition in THP-1 cells. Reactive Oxygen Species 45-48 mitogen-activated protein kinase 8 Homo sapiens 59-62 22096572-0 2011 Fucoidan extract induces apoptosis in MCF-7 cells via a mechanism involving the ROS-dependent JNK activation and mitochondria-mediated pathways. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 8 Homo sapiens 94-97 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 8 Homo sapiens 180-183 20920557-5 2010 The same results were obtained in the cells treated with N-acetyl-L-cysteine, suggesting that the prolonged activation of JNK and p38 by ISA is mediated by reactive oxygen species generated from mitochondria. Reactive Oxygen Species 156-179 mitogen-activated protein kinase 8 Homo sapiens 122-125 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 8 Homo sapiens 146-152 20840847-0 2010 3,6-Dihydroxyflavone induces apoptosis in leukemia HL-60 cell via reactive oxygen species-mediated p38 MAPK/JNK pathway. Reactive Oxygen Species 66-89 mitogen-activated protein kinase 8 Homo sapiens 108-111 20932751-7 2010 Taken together, these data suggest that CWJ-081 induces apoptosis via the mitochondrial apoptotic pathway in HL-60 cells, and ROS-mediated JNK activation plays a key role in the CWJ-081-induced apoptosis. Reactive Oxygen Species 126-129 mitogen-activated protein kinase 8 Homo sapiens 139-142 20736062-7 2010 SOD1 suppressed the increase in c-jun phosphorylation, suggesting that JNK signaling regulates Bax translocation to mitochondria via ROS. Reactive Oxygen Species 133-136 mitogen-activated protein kinase 8 Homo sapiens 71-74 20647313-0 2010 The effects of palmitate on hepatic insulin resistance are mediated by NADPH Oxidase 3-derived reactive oxygen species through JNK and p38MAPK pathways. Reactive Oxygen Species 95-118 mitogen-activated protein kinase 8 Homo sapiens 127-130 20696242-2 2010 Given the relevance of p38 and JNK kinases in stress-response, their activation in fibroblasts from a spectrum of patients (mut, cblA, cblB, cblC and cblE) was analyzed revealing an increased expression of the phosphorylated-forms, specially in cblB and cblC cell lines that presented the highest ROS and apoptosis levels. Reactive Oxygen Species 297-300 mitogen-activated protein kinase 8 Homo sapiens 31-34 20580989-6 2010 Moreover, the mitogen-activated protein kinases (MAPK), the downstream effect of ROS accumulation including c-Jun N-terminal kinase (JNK) and p38 MAPK, could be activated by LYG-202. Reactive Oxygen Species 81-84 mitogen-activated protein kinase 8 Homo sapiens 108-131 20580989-6 2010 Moreover, the mitogen-activated protein kinases (MAPK), the downstream effect of ROS accumulation including c-Jun N-terminal kinase (JNK) and p38 MAPK, could be activated by LYG-202. Reactive Oxygen Species 81-84 mitogen-activated protein kinase 8 Homo sapiens 133-136 20974135-6 2010 Generation of reactive oxygen species (ROS) induced sustained JNK phosphorylation by inactivation of MAP kinase phosphatase 7 (MKP7). Reactive Oxygen Species 14-37 mitogen-activated protein kinase 8 Homo sapiens 62-65 20974135-6 2010 Generation of reactive oxygen species (ROS) induced sustained JNK phosphorylation by inactivation of MAP kinase phosphatase 7 (MKP7). Reactive Oxygen Species 39-42 mitogen-activated protein kinase 8 Homo sapiens 62-65 20727582-8 2010 Moreover, inhibition of ROS attenuated silica nanoparticles-induced apoptosis and inflammation and the activation of JNK, c-Jun, p53 and NF-kappaB. Reactive Oxygen Species 24-27 mitogen-activated protein kinase 8 Homo sapiens 117-120 20647313-10 2010 In conclusion, our data demonstrate a critical role of NOX3-derived ROS in palmitate-induced insulin resistance in hepatocytes, indicating that NOX3 is the predominant source of palmitate-induced ROS generation and that NOX3-derived ROS may drive palmitate-induced hepatic insulin resistance through JNK and p38(MAPK) pathways. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 300-303 20138622-6 2010 N-acetylcysteine that downregulated TNF-alpha-induced reactive oxygen species (ROS) inhibited JNK activation, but not p38 MAPK. Reactive Oxygen Species 54-77 mitogen-activated protein kinase 8 Homo sapiens 94-97 21038848-4 2010 In this study, we found that DADS-induced apoptosis in human leukemia HL-60 cells is mediated by ROS-activated JNK. Reactive Oxygen Species 97-100 mitogen-activated protein kinase 8 Homo sapiens 111-114 21038848-11 2010 These results suggest that JNK is involved in DADS-induced ROS-mediated apoptosis in HL-60 cells. Reactive Oxygen Species 59-62 mitogen-activated protein kinase 8 Homo sapiens 27-30 20138622-10 2010 CONCLUSION: MPA attenuated TNF-alpha-induced ET-1 production through inhibitions of ROS-dependent JNK and ROS-independent p38 MAPK that regulated NF-kappaB as well as AP-1. Reactive Oxygen Species 84-87 mitogen-activated protein kinase 8 Homo sapiens 98-101 20534739-9 2010 Moreover, JNK activation was the earliest response to ATO, preceding and determining reactive oxygen species production. Reactive Oxygen Species 85-108 mitogen-activated protein kinase 8 Homo sapiens 10-13 20438840-8 2010 It was further presented that the higher uptake efficiency, more reactive oxygen species (ROS) generation, and the stronger activation of ROS-dependent c-Jun NH(2)-terminal kinase (JNK) and caspase-3 were induced by the equivalent dose of Tet delivered by nanoparticles. Reactive Oxygen Species 65-88 mitogen-activated protein kinase 8 Homo sapiens 181-184 20438840-8 2010 It was further presented that the higher uptake efficiency, more reactive oxygen species (ROS) generation, and the stronger activation of ROS-dependent c-Jun NH(2)-terminal kinase (JNK) and caspase-3 were induced by the equivalent dose of Tet delivered by nanoparticles. Reactive Oxygen Species 90-93 mitogen-activated protein kinase 8 Homo sapiens 181-184 20438840-8 2010 It was further presented that the higher uptake efficiency, more reactive oxygen species (ROS) generation, and the stronger activation of ROS-dependent c-Jun NH(2)-terminal kinase (JNK) and caspase-3 were induced by the equivalent dose of Tet delivered by nanoparticles. Reactive Oxygen Species 138-141 mitogen-activated protein kinase 8 Homo sapiens 152-179 20438840-8 2010 It was further presented that the higher uptake efficiency, more reactive oxygen species (ROS) generation, and the stronger activation of ROS-dependent c-Jun NH(2)-terminal kinase (JNK) and caspase-3 were induced by the equivalent dose of Tet delivered by nanoparticles. Reactive Oxygen Species 138-141 mitogen-activated protein kinase 8 Homo sapiens 181-184 20435848-9 2010 Meanwhile, resistin activated the mitogen-activated protein kinases p38 and c-Jun NH(2)-terminal kinase (JNK), and the specific p38 inhibitor SB-239063 effectively blocked resistin-induced ROS production and eNOS downregulation. Reactive Oxygen Species 189-192 mitogen-activated protein kinase 8 Homo sapiens 105-108 20138622-6 2010 N-acetylcysteine that downregulated TNF-alpha-induced reactive oxygen species (ROS) inhibited JNK activation, but not p38 MAPK. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 94-97 20590610-8 2010 Two ROS scavengers reduced doxycycline-induced JNK and caspase activation, and apoptosis. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 47-50 20381862-6 2010 JNK activation was due to significantly elevated levels of reactive oxygen species, whereas no TNF-alpha was produced by the macrophages treated with nanoparticles. Reactive Oxygen Species 59-82 mitogen-activated protein kinase 8 Homo sapiens 0-3 20381862-7 2010 Compared to SPIO, USPIO induced more pronounced biochemical alterations and cytotoxicity, which could be antagonized by the JNK inhibitor V. Alternatively, treatment of macrophages with Trolox or N-acetyl-L-cysteine, two functionally different scavengers of reactive oxygen species, abolished both the JNK activation and the subsequent cytotoxic effects. Reactive Oxygen Species 258-281 mitogen-activated protein kinase 8 Homo sapiens 124-127 20590610-9 2010 Taken together, the results suggest the involvement of a ROS-ASK1-JNK pathway in doxycycline-induced melanoma cell apoptosis. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 8 Homo sapiens 66-69 20652490-4 2010 We particularly discuss the role of sustained JNK activation potentiated by ROS, which generally is supportive of apoptosis and "necrotic cell death" through various mechanisms, while ROS could have inhibitory or stimulatory roles in NF-kappaB signaling. Reactive Oxygen Species 76-79 mitogen-activated protein kinase 8 Homo sapiens 46-49 20446899-2 2010 This study suggested that G2/M cell cycle arrest was triggered by ROS/NO productions with regulations of p53, p21, cell division cycle 25C (Cdc25C), Cdc2 and cyclin B1, which were able to be prevented by protein tyrosine kinase (PTK) activity inhibitor genistein or JNK inhibitor SP600125. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Homo sapiens 266-269 20144638-8 2010 Taken together, our data suggest that CMS-9-induced apoptosis of K562 cells is catalytic activity-dependent and is mediated through mitochondria-mediated death pathway triggered by Ca2+/ROS-evoked p38 MAPK and JNK activation. Reactive Oxygen Species 186-189 mitogen-activated protein kinase 8 Homo sapiens 210-213 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 8 Homo sapiens 94-98 20097850-5 2010 The stimulation of oxygen radical generation by S. aureus was dependent on the JNK signaling pathway, as was the phagocytosis of serum-opsonized bacteria. Reactive Oxygen Species 19-33 mitogen-activated protein kinase 8 Homo sapiens 79-82 20230822-4 2010 We explored the possibility that HCV infection regulates TGF-beta1 expression through the generation of reactive oxygen species (ROS), which act through > or =1 of the p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor kappaB (NFkappaB) signaling pathways to induce TGF-beta1 expression. Reactive Oxygen Species 104-127 mitogen-activated protein kinase 8 Homo sapiens 286-289 20230822-4 2010 We explored the possibility that HCV infection regulates TGF-beta1 expression through the generation of reactive oxygen species (ROS), which act through > or =1 of the p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor kappaB (NFkappaB) signaling pathways to induce TGF-beta1 expression. Reactive Oxygen Species 129-132 mitogen-activated protein kinase 8 Homo sapiens 286-289 20398386-4 2010 Because JNK is frequently activated by oxidative stress in cells, we hypothesized that reactive oxygen species (ROS) may be involved in the suppression of JNK dephosphorylation and the cytotoxicity of NSC-741909. Reactive Oxygen Species 87-110 mitogen-activated protein kinase 8 Homo sapiens 8-11 20026682-4 2010 Hypersumoylation in response to modest levels of ROS requires activation of the JNK pathway. Reactive Oxygen Species 49-52 mitogen-activated protein kinase 8 Homo sapiens 80-83 20026682-5 2010 Although ROS-dependent JNK signaling is disabled on decidualization, the cells continue to mount a transcriptional response, albeit distinct from that observed in undifferentiated HESCs. Reactive Oxygen Species 9-12 mitogen-activated protein kinase 8 Homo sapiens 23-26 20026682-8 2010 Thus, JNK silencing uncouples ROS signaling from the SUMO conjugation pathway and maintains progesterone responses and cellular homeostasis in decidual cells under oxidative stress conditions imposed by pregnancy. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Homo sapiens 6-9 21472273-5 2010 JNK inhibitor also somewhat suppressed cell growth inhibition, MMP (Deltapsim) loss and GSH depletion induced by GA, and limited the increase in ROS levels. Reactive Oxygen Species 145-148 mitogen-activated protein kinase 8 Homo sapiens 0-3 20398386-4 2010 Because JNK is frequently activated by oxidative stress in cells, we hypothesized that reactive oxygen species (ROS) may be involved in the suppression of JNK dephosphorylation and the cytotoxicity of NSC-741909. Reactive Oxygen Species 87-110 mitogen-activated protein kinase 8 Homo sapiens 155-158 20398386-4 2010 Because JNK is frequently activated by oxidative stress in cells, we hypothesized that reactive oxygen species (ROS) may be involved in the suppression of JNK dephosphorylation and the cytotoxicity of NSC-741909. Reactive Oxygen Species 112-115 mitogen-activated protein kinase 8 Homo sapiens 8-11 20398386-4 2010 Because JNK is frequently activated by oxidative stress in cells, we hypothesized that reactive oxygen species (ROS) may be involved in the suppression of JNK dephosphorylation and the cytotoxicity of NSC-741909. Reactive Oxygen Species 112-115 mitogen-activated protein kinase 8 Homo sapiens 155-158 20398386-10 2010 Moreover, the NSC-741909-induced ROS generation could be blocked by pretreatment with antioxidants, such as nordihydroguaiaretic acid, aesculetin, baicalein, and caffeic acid, which in turn, inhibited the NSC-741909-induced JNK activation and apoptosis. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 224-227 20227042-4 2010 These effects of IKKbeta/NF-kappaB were cell autonomous and correlated with increased accumulation of reactive oxygen species that led to JNK and STAT3 activation. Reactive Oxygen Species 102-125 mitogen-activated protein kinase 8 Homo sapiens 138-141 24281075-8 2010 Besides causing DNA damage, ROS may further induce multiple intracellular signaling pathways, notably NF-kB, JNK/SAPK/p38, as well as Erk/MAPK. Reactive Oxygen Species 28-31 mitogen-activated protein kinase 8 Homo sapiens 109-112 20102709-0 2010 NOX3-derived reactive oxygen species promote TNF-alpha-induced reductions in hepatocyte glycogen levels via a JNK pathway. Reactive Oxygen Species 13-36 mitogen-activated protein kinase 8 Homo sapiens 110-113 19883629-7 2010 Furthermore, the increase in the phosphorylation of JNK was accompanied by an increase in the reactive oxygen species. Reactive Oxygen Species 94-117 mitogen-activated protein kinase 8 Homo sapiens 52-55 20102709-6 2010 In conclusion, the effects of TNF-alpha on hepatic insulin resistance appear to be, at least in part, mediated by NOX3-derived ROS through a JNK pathway. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 141-144 19882352-0 2010 Reactive oxygen species mediate thymoquinone-induced apoptosis and activate ERK and JNK signaling. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 84-87 19954742-0 2010 Surfactin induces apoptosis in human breast cancer MCF-7 cells through a ROS/JNK-mediated mitochondrial/caspase pathway. Reactive Oxygen Species 73-76 mitogen-activated protein kinase 8 Homo sapiens 77-80 19954742-12 2010 Taken together, these findings suggest that the surfactin induces apoptosis through a ROS/JNK-mediated mitochondrial/caspase pathway. Reactive Oxygen Species 86-89 mitogen-activated protein kinase 8 Homo sapiens 90-93 19887452-7 2010 Although JNK is activated by ROS, this pathway is not associated with cellular senescence of chondrocytes. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 8 Homo sapiens 9-12 19777565-0 2010 Rotenone induces apoptosis in MCF-7 human breast cancer cell-mediated ROS through JNK and p38 signaling. Reactive Oxygen Species 70-73 mitogen-activated protein kinase 8 Homo sapiens 82-85 19855432-0 2010 Prevention of premature senescence requires JNK regulation of Bcl-2 and reactive oxygen species. Reactive Oxygen Species 72-95 mitogen-activated protein kinase 8 Homo sapiens 44-47 19855432-4 2010 Treatment of cells with the JNK-specific inhibitor SP600125 caused phenotypical changes of senescence and triggered a rapid increase in mitochondrial reactive oxygen species (ROS) production and DNA-damage response (DDR) in MCF7 breast carcinoma cells. Reactive Oxygen Species 150-173 mitogen-activated protein kinase 8 Homo sapiens 28-31 19855432-4 2010 Treatment of cells with the JNK-specific inhibitor SP600125 caused phenotypical changes of senescence and triggered a rapid increase in mitochondrial reactive oxygen species (ROS) production and DNA-damage response (DDR) in MCF7 breast carcinoma cells. Reactive Oxygen Species 175-178 mitogen-activated protein kinase 8 Homo sapiens 28-31 19855432-9 2010 Altogether, our results showed that loss of JNK activity triggers a Bcl-2/ROS/DDR signaling cascade that ultimately leads to premature senescence, indicating that basal JNK activity is essential in preventing premature senescence. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 44-47 19855432-9 2010 Altogether, our results showed that loss of JNK activity triggers a Bcl-2/ROS/DDR signaling cascade that ultimately leads to premature senescence, indicating that basal JNK activity is essential in preventing premature senescence. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 169-172 19714450-7 2010 JNK inhibitor also increased cell death, MMP (Delta Psi m) loss, and ROS levels in these cells. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 8 Homo sapiens 0-3 19751824-4 2009 ROS signaling inhibited Nur77 transactivation, which was diminished by either treatment with c-Jun N-terminal kinase (JNK) inhibitor or the expression of a dominant negative form of JNK. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 118-121 19751824-4 2009 ROS signaling inhibited Nur77 transactivation, which was diminished by either treatment with c-Jun N-terminal kinase (JNK) inhibitor or the expression of a dominant negative form of JNK. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 182-185 19549704-11 2009 Blocking ROS generation with N-acetyl-L-cysteine (NAC) significantly prevented GSH depletion and activation of ERK and JNK but not P38. Reactive Oxygen Species 9-12 mitogen-activated protein kinase 8 Homo sapiens 119-122 19846917-9 2009 In addition, the JNK and p38 inhibitors significantly increased the ROS levels including O(2)(-) in the ATO-treated Calu-6 cells. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 17-20 19486916-10 2009 According to these results, we suggest that apoptosis induced by K5 is JNK-dependent and mediated by ROS, but apoptosis induced by staurosporine is not dependent on JNK and that the observed ROS generation by staurosporine seems not to be involved in the activation of this signaling pathway. Reactive Oxygen Species 101-104 mitogen-activated protein kinase 8 Homo sapiens 71-74 19486916-10 2009 According to these results, we suggest that apoptosis induced by K5 is JNK-dependent and mediated by ROS, but apoptosis induced by staurosporine is not dependent on JNK and that the observed ROS generation by staurosporine seems not to be involved in the activation of this signaling pathway. Reactive Oxygen Species 191-194 mitogen-activated protein kinase 8 Homo sapiens 71-74 19361274-5 2009 ROS are important in mediating the sustained activation of JNK, to help mediate apoptosis after TNF treatment. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 59-62 19801848-9 2009 These results indicate that costunolide-induced JNK activation acts downstream of ROS but upstream of Bcl-2, and suggest that ROS-mediated JNK activation plays a key role in costunolide-induced apoptosis. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 48-51 19801848-9 2009 These results indicate that costunolide-induced JNK activation acts downstream of ROS but upstream of Bcl-2, and suggest that ROS-mediated JNK activation plays a key role in costunolide-induced apoptosis. Reactive Oxygen Species 126-129 mitogen-activated protein kinase 8 Homo sapiens 48-51 19801848-9 2009 These results indicate that costunolide-induced JNK activation acts downstream of ROS but upstream of Bcl-2, and suggest that ROS-mediated JNK activation plays a key role in costunolide-induced apoptosis. Reactive Oxygen Species 126-129 mitogen-activated protein kinase 8 Homo sapiens 139-142 19574249-5 2009 We also showed that c-Jun N-terminal kinase (JNK) is involved in ROS-dependent Bax activation. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 8 Homo sapiens 20-43 19574249-5 2009 We also showed that c-Jun N-terminal kinase (JNK) is involved in ROS-dependent Bax activation. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 8 Homo sapiens 45-48 19574249-11 2009 These results indicate that the natural triterpenoid pristimerin induces mitochondrial cell death through ROS-dependent activation of both Bax and PARP-1 in human cervical cancer cells and that JNK is involved in ROS-dependent Bax activation. Reactive Oxygen Species 213-216 mitogen-activated protein kinase 8 Homo sapiens 194-197 18681908-6 2009 We observed that reactive oxygen species-mediated JNK activation is involved in this SIRT1 down-regulation. Reactive Oxygen Species 17-40 mitogen-activated protein kinase 8 Homo sapiens 50-53 19652370-8 2009 In addition, we also showed that berberine could activate phosphoinositide-3 kinase (PI3K)/Akt and that pretreatment with PI3K/Akt inhibitors prevented berberine-induced inhibition of ROS, JNK and subsequent apoptosis, suggesting that the protective effects of berberine were PI3K/Akt-dependent. Reactive Oxygen Species 184-187 mitogen-activated protein kinase 8 Homo sapiens 189-192 19468286-2 2009 The present study further demonstrates that reactive oxygen species (ROS) were generated in abundance in Jurkat leukemia cells upon AD5-10 stimulation and that ROS accumulation subsequently evoked sustained activation of c-Jun N-terminal kinase (JNK), loss of mitochondrial membrane potential, and release of endonuclease G (Endo G) from mitochondria into the cytosol. Reactive Oxygen Species 69-72 mitogen-activated protein kinase 8 Homo sapiens 246-249 19468286-2 2009 The present study further demonstrates that reactive oxygen species (ROS) were generated in abundance in Jurkat leukemia cells upon AD5-10 stimulation and that ROS accumulation subsequently evoked sustained activation of c-Jun N-terminal kinase (JNK), loss of mitochondrial membrane potential, and release of endonuclease G (Endo G) from mitochondria into the cytosol. Reactive Oxygen Species 160-163 mitogen-activated protein kinase 8 Homo sapiens 221-244 19468286-2 2009 The present study further demonstrates that reactive oxygen species (ROS) were generated in abundance in Jurkat leukemia cells upon AD5-10 stimulation and that ROS accumulation subsequently evoked sustained activation of c-Jun N-terminal kinase (JNK), loss of mitochondrial membrane potential, and release of endonuclease G (Endo G) from mitochondria into the cytosol. Reactive Oxygen Species 160-163 mitogen-activated protein kinase 8 Homo sapiens 246-249 19325135-0 2009 PLAB induction in fenretinide-induced apoptosis of ovarian cancer cells occurs via a ROS-dependent mechanism involving ER stress and JNK activation. Reactive Oxygen Species 85-88 mitogen-activated protein kinase 8 Homo sapiens 133-136 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 8 Homo sapiens 53-56 19277946-6 2009 The JNK inhibitor, SP600125, attenuated insulin resistance mediated by SFA and Tlr agonists, which corresponded with a diminished proinflammatory response and reduced ROS accumulation. Reactive Oxygen Species 167-170 mitogen-activated protein kinase 8 Homo sapiens 4-7 19292871-4 2009 Activation of JNK by morphine led to reactive oxygen species (ROS) generation via the mitochondrial permeability transition pore, because the mPTP inhibitor cyclosporin A significantly inhibited ROS generation. Reactive Oxygen Species 37-60 mitogen-activated protein kinase 8 Homo sapiens 14-17 19673930-10 2009 The results of the present study suggest that erlotinib has potent antitumour activity in A549 cells by activating ROS-dependent, JNK-driven cell apoptosis. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 8 Homo sapiens 130-133 19292871-4 2009 Activation of JNK by morphine led to reactive oxygen species (ROS) generation via the mitochondrial permeability transition pore, because the mPTP inhibitor cyclosporin A significantly inhibited ROS generation. Reactive Oxygen Species 62-65 mitogen-activated protein kinase 8 Homo sapiens 14-17 19292871-9 2009 Thus, the present study clearly shows that morphine-induced apoptosis in SH-SY5Y cells involves JNK-dependent activation of the mitochondrial death pathway, and that ROS signaling exerts positive feedback regulation of JNK activity. Reactive Oxygen Species 166-169 mitogen-activated protein kinase 8 Homo sapiens 219-222 19292871-4 2009 Activation of JNK by morphine led to reactive oxygen species (ROS) generation via the mitochondrial permeability transition pore, because the mPTP inhibitor cyclosporin A significantly inhibited ROS generation. Reactive Oxygen Species 195-198 mitogen-activated protein kinase 8 Homo sapiens 14-17 19292871-5 2009 ROS in turn exerted feedback regulation on JNK activation, as shown by the observations that cyclosporin A and the antioxidant N-acetylcysteine significantly inhibited the phosphorylation of JNK induced by morphine. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 43-46 19292871-5 2009 ROS in turn exerted feedback regulation on JNK activation, as shown by the observations that cyclosporin A and the antioxidant N-acetylcysteine significantly inhibited the phosphorylation of JNK induced by morphine. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 191-194 19292871-6 2009 ROS-amplified JNK induced cytochrome c release and caspase-9/3 activation through enhancement of expression of the proapoptotic protein Bim and reduction of expression of the antiapoptotic protein Bcl-2. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 14-17 18805632-5 2009 ROS activated almost immediately in a time- and concentration-dependent manner the MAPK pathways p38, ERK and JNK (their activation was abrogated by the antioxidant N-acetylcysteine). Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 110-113 19037093-7 2009 Our data further showed that AMPK relayed a survival signal transmitted by early activation of JNK and that the sustained AMPK signal in turn inhibited the proapoptotic property of JNK via a negative feedback mechanism involving reactive oxygen species. Reactive Oxygen Species 229-252 mitogen-activated protein kinase 8 Homo sapiens 181-184 19118896-4 2009 Experiments studying placental ischaemia-reperfusion in vitro or in vivo during labour provide strong evidence suggesting that oxidative stress and ROS production can activate downstream stress-signalling pathways, p38 and SAPK/JNK MAPK, and the pro-inflammatory NF-kappaB signalling pathway, culminating in the release of inflammatory mediators, apoptotic debris, anti-angiogenic factors and other mediators, which then stimulate a maternal inflammatory reaction that manifests in endothelial dysfunction and the symptoms of pre-eclampsia. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Homo sapiens 228-231 18606492-10 2008 These results suggest that the ROS-ASK1-p38/JNK-p53 and Bax pathway plays a critical role in HBI"s anti-cancer effects. Reactive Oxygen Species 31-34 mitogen-activated protein kinase 8 Homo sapiens 44-47 18692129-7 2008 The data indicate that activation of JNK1/AP-1 and subsequent IL-8 induction in hyperoxia are mediated by intracellular ROS, with SOD having significant protective effects. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 37-41 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 8 Homo sapiens 149-152 18281123-10 2008 In conclusion, in H1299 human NSCLC cells, sulindac and ATO synergistically induce a high degree of apoptosis, which is mediated by the ROS-dependent JNK activation pathway via Bcl-xL phosphorylation. Reactive Oxygen Species 136-139 mitogen-activated protein kinase 8 Homo sapiens 150-153 18618576-11 2008 Note that 3-indole-induced JNK activation and DNA damage can be partially suppressed by an ROS inhibitor. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 8 Homo sapiens 27-30 18618576-12 2008 Apoptosis induced by 3-indole could be abrogated by ROS or JNK inhibitors, suggesting the importance of ROS and JNK stress-related pathways in 3-indole-induced apoptosis. Reactive Oxygen Species 52-55 mitogen-activated protein kinase 8 Homo sapiens 112-115 18618576-12 2008 Apoptosis induced by 3-indole could be abrogated by ROS or JNK inhibitors, suggesting the importance of ROS and JNK stress-related pathways in 3-indole-induced apoptosis. Reactive Oxygen Species 104-107 mitogen-activated protein kinase 8 Homo sapiens 59-62 18728404-3 2008 In this study, we showed that selenite-induced apoptosis in HepG2 cells was mediated by ROS that activated JNK to regulate apoptosis. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 8 Homo sapiens 107-110 18728404-9 2008 These results revealed that JNK might be involved in selenite-induced ROS-mediated apoptosis in HepG2 cells. Reactive Oxygen Species 70-73 mitogen-activated protein kinase 8 Homo sapiens 28-31 18398104-3 2008 The synthetic cytotoxic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) is known to generate reactive oxygen species (ROS), and ROS have been shown to activate c-Jun kinase (JNK), which in turn phosphorylates and inhibits Mcl-1. Reactive Oxygen Species 92-115 mitogen-activated protein kinase 8 Homo sapiens 159-171 18398104-3 2008 The synthetic cytotoxic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) is known to generate reactive oxygen species (ROS), and ROS have been shown to activate c-Jun kinase (JNK), which in turn phosphorylates and inhibits Mcl-1. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 159-171 18398104-3 2008 The synthetic cytotoxic retinoid N-(4-hydroxyphenyl)retinamide (4-HPR) is known to generate reactive oxygen species (ROS), and ROS have been shown to activate c-Jun kinase (JNK), which in turn phosphorylates and inhibits Mcl-1. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 173-176 18324519-5 2008 Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 8 Homo sapiens 201-204 18840412-0 2008 Glibenclamide exerts an antitumor activity through reactive oxygen species-c-jun NH2-terminal kinase pathway in human gastric cancer cell line MGC-803. Reactive Oxygen Species 51-74 mitogen-activated protein kinase 8 Homo sapiens 75-100 18840412-8 2008 Taken together, our study reveals that glibenclamide exerts an antitumor activity in MGC-803 cells by activating ROS-dependent, JNK-driven cell apoptosis. Reactive Oxygen Species 113-116 mitogen-activated protein kinase 8 Homo sapiens 128-131 18923045-6 2008 NMDAR-dependent pro-death signaling via p38 relies on neuronal context, although death signaling by JNK, triggered by mitochondrial reactive oxygen species production, does not. Reactive Oxygen Species 132-155 mitogen-activated protein kinase 8 Homo sapiens 100-103 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 8 Homo sapiens 94-97 18412143-10 2008 These results support a notion that ROS-mediated activations of p38 MAPK and JNK in response to As2O3 treatment signals activation of Bax and phosphorylation of Bcl-2, resulting in mitochondrial apoptotic cell death in human cervical cancer cells. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 77-80 18281123-4 2008 The c-Jun NH(2)-terminal kinase (JNK) was activated downstream of ROS production in H1299 cells. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Homo sapiens 4-31 18281123-4 2008 The c-Jun NH(2)-terminal kinase (JNK) was activated downstream of ROS production in H1299 cells. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Homo sapiens 33-36 18691550-1 2008 Hepatocyte I kappaB kinase beta (IKK beta) inhibits hepatocarcinogenesis by suppressing accumulation of reactive oxygen species (ROS) and liver damage, whereas JNK1 activation promotes ROS accumulation, liver damage, and carcinogenesis. Reactive Oxygen Species 185-188 mitogen-activated protein kinase 8 Homo sapiens 160-164 18663379-3 2008 Scavenging of ROS completely blocked all of the above-mentioned events (i.e., JNK and p38 phosphorylation, cytochrome c and Smac/DIABLO release, caspase and PARP cleavage, as well as the induction of apoptosis) following shikonin treatment. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 78-81 18403484-8 2008 Interestingly, dexamethasone induces the generation of reactive oxygen species (measured by dihydrofluorescein assay), which participate in the signaling process by triggering JNK activation. Reactive Oxygen Species 55-78 mitogen-activated protein kinase 8 Homo sapiens 176-179 18569013-8 2008 These results suggested that ROS generation through Cr(VI) treatment cause ER stress, JNK activation and insulin resistance in adipocytes. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 8 Homo sapiens 86-89 18569016-5 2008 ROS induced by chronic insulin treatment inhibited insulin signalling and glucose uptake, induced endoplasmic reticulum (ER) stress and JNK activation. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 136-139 18566239-3 2008 Previously, we described the requirement for a reactive oxygen species-mediated, SEK1/c-Jun NH2-terminal kinase (JNK) pathway to induce apoptosis. Reactive Oxygen Species 47-70 mitogen-activated protein kinase 8 Homo sapiens 113-116 18374381-11 2008 The ROS/JNK pathway could be a useful target for novel approaches in breast cancer chemotherapy. Reactive Oxygen Species 4-7 mitogen-activated protein kinase 8 Homo sapiens 8-11 18262755-4 2008 This resulted in a promotion of mitochondrial ROS production, which was found to be induced via sequential actions of c-Jun N-terminal kinase (JNK), Bax, and caspase-3. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 118-141 18262755-4 2008 This resulted in a promotion of mitochondrial ROS production, which was found to be induced via sequential actions of c-Jun N-terminal kinase (JNK), Bax, and caspase-3. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 143-146 18262755-5 2008 Interestingly, the induced ROS, in turn, re-activated JNK, Bax, and caspase-3 in the same model system. Reactive Oxygen Species 27-30 mitogen-activated protein kinase 8 Homo sapiens 54-57 18262755-6 2008 Consistently, the blockade of Bax action by RNA interference or Bcl-2 overexpression abolished the activation of JNK induced after, but not before, the production of ROS. Reactive Oxygen Species 166-169 mitogen-activated protein kinase 8 Homo sapiens 113-116 18262755-8 2008 Functional analyses revealed that the initial ROS-independent activations of JNK, Bax, and caspase-3 are not sufficient for cell death, and thus, should be re-activated by ROS in order to kill the cells. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 77-80 18262755-8 2008 Functional analyses revealed that the initial ROS-independent activations of JNK, Bax, and caspase-3 are not sufficient for cell death, and thus, should be re-activated by ROS in order to kill the cells. Reactive Oxygen Species 172-175 mitogen-activated protein kinase 8 Homo sapiens 77-80 18262755-9 2008 These findings suggest that ROS do not simply mediate the lethal action of gamma-irradiation, but actually amplify it by forming a feedback loop between a downstream effector caspase and the upstream initiation signals leading to the activation of JNK. Reactive Oxygen Species 28-31 mitogen-activated protein kinase 8 Homo sapiens 248-251 18398104-13 2008 Using the antioxidant ascorbic acid and siRNA-mediated knockdown of JNK, we showed that 4-HPR decreased Mcl-1 via ROS generation (that phosphorylates JNK) in ABT-737-resistant cell lines. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Homo sapiens 68-71 18398104-13 2008 Using the antioxidant ascorbic acid and siRNA-mediated knockdown of JNK, we showed that 4-HPR decreased Mcl-1 via ROS generation (that phosphorylates JNK) in ABT-737-resistant cell lines. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Homo sapiens 150-153 18218673-1 2008 Previously we have shown that both Rac1 and c-Jun NH(2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive oxygen species (ROS) in apoptosis is unclear. Reactive Oxygen Species 239-262 mitogen-activated protein kinase 8 Homo sapiens 73-79 18218673-1 2008 Previously we have shown that both Rac1 and c-Jun NH(2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive oxygen species (ROS) in apoptosis is unclear. Reactive Oxygen Species 264-267 mitogen-activated protein kinase 8 Homo sapiens 73-79 18219313-0 2008 NLRX1 is a mitochondrial NOD-like receptor that amplifies NF-kappaB and JNK pathways by inducing reactive oxygen species production. Reactive Oxygen Species 97-120 mitogen-activated protein kinase 8 Homo sapiens 72-75 18305405-12 2008 Furthermore, p38 and JNK but not ERK were activated by proton and dominant negative mutants of p38 and JNK revived proton-induced apoptosis, suggesting that p38 and JNK pathway may be activated through ROS to activate apoptosis. Reactive Oxygen Species 202-205 mitogen-activated protein kinase 8 Homo sapiens 21-24 18305405-12 2008 Furthermore, p38 and JNK but not ERK were activated by proton and dominant negative mutants of p38 and JNK revived proton-induced apoptosis, suggesting that p38 and JNK pathway may be activated through ROS to activate apoptosis. Reactive Oxygen Species 202-205 mitogen-activated protein kinase 8 Homo sapiens 103-106 18305405-12 2008 Furthermore, p38 and JNK but not ERK were activated by proton and dominant negative mutants of p38 and JNK revived proton-induced apoptosis, suggesting that p38 and JNK pathway may be activated through ROS to activate apoptosis. Reactive Oxygen Species 202-205 mitogen-activated protein kinase 8 Homo sapiens 103-106 18068334-8 2008 Pretreatment of melanoma cells with the JNK inhibitor (SP600125) or the p38 inhibitor (SB203580) blocked taxol-induced UCP2 downregulation, ROS generation and apoptosis, whereas the ERK inhibitor (PD98059) had no such effect. Reactive Oxygen Species 140-143 mitogen-activated protein kinase 8 Homo sapiens 40-43 18199537-6 2008 Mechanistic analysis indicated that GLIPR1 up-regulation increases the production of reactive oxygen species (ROS) leading to apoptosis through activation of the c-Jun-NH(2) kinase (JNK) signaling cascade. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 8 Homo sapiens 162-180 18199537-6 2008 Mechanistic analysis indicated that GLIPR1 up-regulation increases the production of reactive oxygen species (ROS) leading to apoptosis through activation of the c-Jun-NH(2) kinase (JNK) signaling cascade. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 8 Homo sapiens 182-185 18199537-7 2008 Thus, our results identify GLIPR1 as a proapoptotic tumor suppressor acting through the ROS-JNK pathway and support the therapeutic potential for this protein. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 8 Homo sapiens 92-95 17939949-0 2008 Toll-like receptor 9-stimulated monocyte chemoattractant protein-1 is mediated via JNK-cytosolic phospholipase A2-ROS signaling. Reactive Oxygen Species 114-117 mitogen-activated protein kinase 8 Homo sapiens 83-86 17881465-9 2007 Together, these data suggest that the ROS-EGFR-JNK pathway is involved in transducing the proliferative effect of ANG II in cultured HMCs. Reactive Oxygen Species 38-41 mitogen-activated protein kinase 8 Homo sapiens 47-50 16963249-10 2007 Our results indicated that DHA-mediated apoptosis in E47 cells was induced through the activation of the JNK-related cell death pathway, which may be involved in the production of LPO or reactive oxygen species during the CYP2E1 catalytic cycle, followed by mitochondrial injury and apoptosis. Reactive Oxygen Species 187-210 mitogen-activated protein kinase 8 Homo sapiens 105-108 17576159-9 2007 The activation of the JNK pathway plays a key role in the induction of cellular death in response to ROS. Reactive Oxygen Species 101-104 mitogen-activated protein kinase 8 Homo sapiens 22-25 17647244-8 2007 RESULTS: Treatment of glioblastoma cells with garlic compounds triggered production of ROS that induced apoptosis with the phosphorylation of p38 MAPK and activation of the redox-sensitive JNK1 pathway. Reactive Oxygen Species 87-90 mitogen-activated protein kinase 8 Homo sapiens 189-193 17603935-0 2007 Tumor necrosis factor-alpha-induced reactive oxygen species formation is mediated by JNK1-dependent ferritin degradation and elevation of labile iron pool. Reactive Oxygen Species 36-59 mitogen-activated protein kinase 8 Homo sapiens 85-89 17603935-3 2007 We hypothesized that TNF-induced ROS formation is due to JNK-regulated ferritin degradation and an increase in labile iron pool (LIP). Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 57-60 17603935-9 2007 The cells expressing inactive JNK1 mutant, but not cells expressing JNK2 mutant or possessing an empty vector, were completely resistant to TNF-induced ROS generation, ferritin degradation, and an increase in LIP. Reactive Oxygen Species 152-155 mitogen-activated protein kinase 8 Homo sapiens 30-34 17603935-10 2007 These data suggest that TNF-induced ROS formation is mediated by JNK1, which regulates ferritin degradation and thus the level of highly reactive iron. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 65-69 17400550-5 2007 Indeed, activation of p38 MAPK and JNK1 mediated by mitochondrial ROS were required for HIF-1alpha phosphorylation and accumulation after UVB irradiation. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Homo sapiens 35-39 18481208-6 2007 RESULTS: Using the anti-oxidants N-acetyl L-cysteine (NAC) and ebselen to deplete intracellular ROS, we identified a differential requirement for ROS in the activation of ERK, JNK, p38, and Akt by these receptors. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 8 Homo sapiens 176-179 18481208-6 2007 RESULTS: Using the anti-oxidants N-acetyl L-cysteine (NAC) and ebselen to deplete intracellular ROS, we identified a differential requirement for ROS in the activation of ERK, JNK, p38, and Akt by these receptors. Reactive Oxygen Species 146-149 mitogen-activated protein kinase 8 Homo sapiens 176-179 18481208-7 2007 We found that CD40 activated JNK, p38, and Akt via redox-dependent pathways that were sensitive to ROS depletion by NAC and ebselen. Reactive Oxygen Species 99-102 mitogen-activated protein kinase 8 Homo sapiens 29-32 18481208-9 2007 We also found that CXCR4-induced Akt activation was ROS-dependent even though activation of the ERK, JNK, and p38 MAP kinases by CXCR4 occurred via ROS-independent pathways. Reactive Oxygen Species 148-151 mitogen-activated protein kinase 8 Homo sapiens 101-104 18481208-10 2007 CONCLUSION: The differential requirement for ROS in the activation of ERK, JNK, p38, and Akt by the BCR, CD40, and CXCR4 likely reflects the multiplicity of upstream activators for each of these kinases, only some of which may be regulated in a redox-dependent manner. Reactive Oxygen Species 45-48 mitogen-activated protein kinase 8 Homo sapiens 75-78 17360708-6 2007 In addition, cyanidin-3-rutinoside treatment resulted in reactive oxygen species (ROS)-dependent activation of p38 MAPK and JNK, which contributed to cell death by activating the mitochondrial pathway mediated by Bim. Reactive Oxygen Species 57-80 mitogen-activated protein kinase 8 Homo sapiens 124-127 17360708-6 2007 In addition, cyanidin-3-rutinoside treatment resulted in reactive oxygen species (ROS)-dependent activation of p38 MAPK and JNK, which contributed to cell death by activating the mitochondrial pathway mediated by Bim. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 124-127 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 8 Homo sapiens 190-196 17296806-7 2007 It is noteworthy that suppression of ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the luteolin-induced suppression of NF-kappaB and potentiation of JNK and significantly suppressed the synergistic cytotoxicity seen with cotreatment of luteolin and TNF. Reactive Oxygen Species 37-40 mitogen-activated protein kinase 8 Homo sapiens 198-201 17296806-7 2007 It is noteworthy that suppression of ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the luteolin-induced suppression of NF-kappaB and potentiation of JNK and significantly suppressed the synergistic cytotoxicity seen with cotreatment of luteolin and TNF. Reactive Oxygen Species 57-60 mitogen-activated protein kinase 8 Homo sapiens 198-201 17296806-8 2007 Taken together, these results suggest that the accumulation of ROS induced by luteolin plays a pivotal role in suppression of NF-kappaB and potentiation of JNK to sensitize lung cancer cells to undergo TNF-induced apoptosis. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 8 Homo sapiens 156-159 17390063-0 2007 Ionizing radiation-induced micronucleus formation is mediated by reactive oxygen species that are produced in a manner dependent on mitochondria, Nox1, and JNK. Reactive Oxygen Species 65-88 mitogen-activated protein kinase 8 Homo sapiens 156-159 17390063-9 2007 SP600125, a JNK-specific inhibitor, suppressed the IR-induced accumulation of ROS. Reactive Oxygen Species 78-81 mitogen-activated protein kinase 8 Homo sapiens 12-15 17308059-12 2007 Thus, DCA and 17AAG interact to stimulate Ca(2+)-dependent and PKR-like endoplasmic reticulum kinase-dependent ROS production; high levels of ROS promote intense activation of the p38 MAPK and JNK1/2 pathways that signal to activate the intrinsic apoptosis pathway. Reactive Oxygen Species 142-145 mitogen-activated protein kinase 8 Homo sapiens 193-199 17121845-8 2007 Thus, sustained JNK activation by TNF has no obligate role in TNF-induced cell death and is mediated by caspases and reactive oxygen species in a cell type-specific manner. Reactive Oxygen Species 117-140 mitogen-activated protein kinase 8 Homo sapiens 16-19 17110930-8 2006 Taken that ROS promote JNK activation and activation of the JNK pathway may promote ROS accumulation, c-FLIPL might block this positive feedback loop, thereby suppressing ROS accumulation. Reactive Oxygen Species 11-14 mitogen-activated protein kinase 8 Homo sapiens 23-26 17875416-7 2007 Hyperosmolarity-induced ROS formation then leads to a Src-family kinase Yes-mediated activation of the epidermal growth factor receptor (EGFR) and to an activation of the c-Jun-N-terminal kinase (JNK). Reactive Oxygen Species 24-27 mitogen-activated protein kinase 8 Homo sapiens 171-194 17875416-7 2007 Hyperosmolarity-induced ROS formation then leads to a Src-family kinase Yes-mediated activation of the epidermal growth factor receptor (EGFR) and to an activation of the c-Jun-N-terminal kinase (JNK). Reactive Oxygen Species 24-27 mitogen-activated protein kinase 8 Homo sapiens 196-199 16973888-1 2006 We show here that Ca(2+) and reactive oxygen species (ROS) are involved in the up-regulation of c-Jun NH(2)-terminal kinase 1 (JNK1) activity during apoptosis induced by ginsenoside Rh2 (G-Rh2) in HeLa, MCF10A-ras, and MCF7 cells. Reactive Oxygen Species 29-52 mitogen-activated protein kinase 8 Homo sapiens 96-125 16973888-1 2006 We show here that Ca(2+) and reactive oxygen species (ROS) are involved in the up-regulation of c-Jun NH(2)-terminal kinase 1 (JNK1) activity during apoptosis induced by ginsenoside Rh2 (G-Rh2) in HeLa, MCF10A-ras, and MCF7 cells. Reactive Oxygen Species 29-52 mitogen-activated protein kinase 8 Homo sapiens 127-131 16973888-1 2006 We show here that Ca(2+) and reactive oxygen species (ROS) are involved in the up-regulation of c-Jun NH(2)-terminal kinase 1 (JNK1) activity during apoptosis induced by ginsenoside Rh2 (G-Rh2) in HeLa, MCF10A-ras, and MCF7 cells. Reactive Oxygen Species 54-57 mitogen-activated protein kinase 8 Homo sapiens 96-125 16973888-1 2006 We show here that Ca(2+) and reactive oxygen species (ROS) are involved in the up-regulation of c-Jun NH(2)-terminal kinase 1 (JNK1) activity during apoptosis induced by ginsenoside Rh2 (G-Rh2) in HeLa, MCF10A-ras, and MCF7 cells. Reactive Oxygen Species 54-57 mitogen-activated protein kinase 8 Homo sapiens 127-131 16973888-6 2006 These results suggest that ROS and Ca(2+) are important signaling intermediates leading to stress-activated protein kinase/extracellular signal-regulated kinase kinase 1/JNK1 activation and depolarization of the mitochondrial membrane potential in G-Rh2-induced apoptosis. Reactive Oxygen Species 27-30 mitogen-activated protein kinase 8 Homo sapiens 170-174 17110930-8 2006 Taken that ROS promote JNK activation and activation of the JNK pathway may promote ROS accumulation, c-FLIPL might block this positive feedback loop, thereby suppressing ROS accumulation. Reactive Oxygen Species 11-14 mitogen-activated protein kinase 8 Homo sapiens 60-63 17110930-8 2006 Taken that ROS promote JNK activation and activation of the JNK pathway may promote ROS accumulation, c-FLIPL might block this positive feedback loop, thereby suppressing ROS accumulation. Reactive Oxygen Species 84-87 mitogen-activated protein kinase 8 Homo sapiens 60-63 17110930-8 2006 Taken that ROS promote JNK activation and activation of the JNK pathway may promote ROS accumulation, c-FLIPL might block this positive feedback loop, thereby suppressing ROS accumulation. Reactive Oxygen Species 84-87 mitogen-activated protein kinase 8 Homo sapiens 60-63 17072325-3 2006 In these pathways, cytotoxic ROS signaling appears to be mediated in part by activation of the c-Jun-N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) cascade. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 8 Homo sapiens 95-118 17023263-2 2006 This study shows that in human keratinocytes exposed to UVB the generation of reactive oxygen species (ROS) acts as a mediator of apoptosis signal regulating kinase-1 (Ask-1), a redox-sensitive mitogen-activated protein kinase kinase kinase (MAP3K) regulating p38 MAPK and JNK cascades. Reactive Oxygen Species 78-101 mitogen-activated protein kinase 8 Homo sapiens 273-276 17023263-2 2006 This study shows that in human keratinocytes exposed to UVB the generation of reactive oxygen species (ROS) acts as a mediator of apoptosis signal regulating kinase-1 (Ask-1), a redox-sensitive mitogen-activated protein kinase kinase kinase (MAP3K) regulating p38 MAPK and JNK cascades. Reactive Oxygen Species 103-106 mitogen-activated protein kinase 8 Homo sapiens 273-276 17072325-3 2006 In these pathways, cytotoxic ROS signaling appears to be mediated in part by activation of the c-Jun-N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) cascade. Reactive Oxygen Species 29-32 mitogen-activated protein kinase 8 Homo sapiens 120-123 17072325-7 2006 Effectors of this antagonistic cross-talk between NF-kappaB and ROS/JNK pathways have recently been identified. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 68-71 16787235-4 2006 Here, we review the molecular signaling pathways involved in Abeta-induced cell death, including signaling through the neuronal nicotinic receptor and the Abeta-triggered generation of reactive oxygen species (ROS) leading to the activation of the c-jun N-terminal kinase (JNK), and the ensuing phosphorylation of p66Shc and inactivation of the Forkhead transcription factors. Reactive Oxygen Species 185-208 mitogen-activated protein kinase 8 Homo sapiens 248-271 16873882-7 2006 Recently, some important discoveries have underscored the critical role of ROS in TNFalpha signaling, notably in TNFalpha-mediated activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (c-Jun NH2-terminal kinase, JNK), as well as in cell death (apoptotic and necrotic) pathways. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 8 Homo sapiens 235-238 16787235-4 2006 Here, we review the molecular signaling pathways involved in Abeta-induced cell death, including signaling through the neuronal nicotinic receptor and the Abeta-triggered generation of reactive oxygen species (ROS) leading to the activation of the c-jun N-terminal kinase (JNK), and the ensuing phosphorylation of p66Shc and inactivation of the Forkhead transcription factors. Reactive Oxygen Species 210-213 mitogen-activated protein kinase 8 Homo sapiens 248-271 16787235-4 2006 Here, we review the molecular signaling pathways involved in Abeta-induced cell death, including signaling through the neuronal nicotinic receptor and the Abeta-triggered generation of reactive oxygen species (ROS) leading to the activation of the c-jun N-terminal kinase (JNK), and the ensuing phosphorylation of p66Shc and inactivation of the Forkhead transcription factors. Reactive Oxygen Species 210-213 mitogen-activated protein kinase 8 Homo sapiens 273-276 16707465-0 2006 c-Jun NH(2)-terminal kinase signaling axis regulates diallyl trisulfide-induced generation of reactive oxygen species and cell cycle arrest in human prostate cancer cells. Reactive Oxygen Species 94-117 mitogen-activated protein kinase 8 Homo sapiens 0-27 16707465-6 2006 Interestingly, DATS-mediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arrest were significantly attenuated by ectopic expression of a catalytically inactive mutant of JNK kinase 2 and RNA interference of stress-activated protein kinase/extracellular signal-regulated kinase 1 (SEK1), upstream kinases in JNK signal transduction pathway. Reactive Oxygen Species 84-87 mitogen-activated protein kinase 8 Homo sapiens 215-218 16707465-2 2006 Using DU145 and PC-3 human prostate cancer cells as a model, we now report a novel mechanism involving c-Jun NH(2)-terminal kinase (JNK) signaling axis, which is known for its role in regulation of cell survival and apoptosis, in DATS-induced ROS production. Reactive Oxygen Species 243-246 mitogen-activated protein kinase 8 Homo sapiens 103-130 16707465-7 2006 In conclusion, the present study provides experimental evidence to indicate existence of a novel pathway involving JNK signaling axis in regulation of DATS-induced ROS generation. Reactive Oxygen Species 164-167 mitogen-activated protein kinase 8 Homo sapiens 115-118 16707465-2 2006 Using DU145 and PC-3 human prostate cancer cells as a model, we now report a novel mechanism involving c-Jun NH(2)-terminal kinase (JNK) signaling axis, which is known for its role in regulation of cell survival and apoptosis, in DATS-induced ROS production. Reactive Oxygen Species 243-246 mitogen-activated protein kinase 8 Homo sapiens 132-135 16407847-10 2006 These data indicate that 4HPR-induced apoptosis is triggered by ROS increase, leading to the activation of the mitogen-activated protein serine/threonine kinases JNK, p38, PKC and ERK, and subsequent apoptosis. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 162-165 16734756-5 2006 This complex process with a NADPH oxidase-derived reactive oxygen species signal as an important upstream event, allows via Yes, JNK and epidermal growth factor-receptor 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 50-73 mitogen-activated protein kinase 8 Homo sapiens 129-132 16341124-0 2006 Reactive oxygen species mediate crosstalk between NF-kappaB and JNK. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 64-67 16651444-7 2006 ROS production, in turn, led to the activation of stress-activated pathways involving p38 and c-Jun NH(2)-terminal kinase. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 94-121 16341124-4 2006 Further studies have also revealed that NF-kappaB inhibits JNK activation by suppressing accumulation of reactive oxygen species (ROS). Reactive Oxygen Species 105-128 mitogen-activated protein kinase 8 Homo sapiens 59-62 16341124-4 2006 Further studies have also revealed that NF-kappaB inhibits JNK activation by suppressing accumulation of reactive oxygen species (ROS). Reactive Oxygen Species 130-133 mitogen-activated protein kinase 8 Homo sapiens 59-62 16341124-5 2006 In this review, we will focus on the signaling crosstalk between the NF-kappaB and JNK cascades via ROS. Reactive Oxygen Species 100-103 mitogen-activated protein kinase 8 Homo sapiens 83-86 16387755-2 2006 The c-Jun NH(2)-terminal kinase (JNK) pathway has been shown to play a critical role in ROS-induced cell death. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 8 Homo sapiens 4-31 16387755-2 2006 The c-Jun NH(2)-terminal kinase (JNK) pathway has been shown to play a critical role in ROS-induced cell death. Reactive Oxygen Species 88-91 mitogen-activated protein kinase 8 Homo sapiens 33-36 16540388-3 2006 Recently there has been an increasing amount of research interest focusing on the regulatory role of JNK activation in ROS-and RNS-induced cellular responses. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 8 Homo sapiens 101-104 16456579-5 2006 This participation of NF-kappaB in survival signaling often involves an antagonism of PCD triggered by TNF-R-family receptors, and is mediated through a suppression of the formation of reactive oxygen species (ROS) and a control of sustained activation of the Jun-N-terminal kinase (JNK) cascade. Reactive Oxygen Species 185-208 mitogen-activated protein kinase 8 Homo sapiens 283-286 16456579-5 2006 This participation of NF-kappaB in survival signaling often involves an antagonism of PCD triggered by TNF-R-family receptors, and is mediated through a suppression of the formation of reactive oxygen species (ROS) and a control of sustained activation of the Jun-N-terminal kinase (JNK) cascade. Reactive Oxygen Species 210-213 mitogen-activated protein kinase 8 Homo sapiens 283-286 16456579-6 2006 Effectors of this antagonistic activity of NF-kappaB on this ROS/JNK pathway have been recently identified. Reactive Oxygen Species 61-64 mitogen-activated protein kinase 8 Homo sapiens 65-68 16515547-7 2006 Furthermore, suppression of the 6-OHDA-generated reactive oxygen species (ROS) by pre-incubation of cells with N-acetyl-L-cysteine effectively inhibited the 6-OHDA-induced activation of ASK1, p38 and JNK, and protected the cells from apoptosis. Reactive Oxygen Species 49-72 mitogen-activated protein kinase 8 Homo sapiens 200-203 16515547-7 2006 Furthermore, suppression of the 6-OHDA-generated reactive oxygen species (ROS) by pre-incubation of cells with N-acetyl-L-cysteine effectively inhibited the 6-OHDA-induced activation of ASK1, p38 and JNK, and protected the cells from apoptosis. Reactive Oxygen Species 74-77 mitogen-activated protein kinase 8 Homo sapiens 200-203 16515547-8 2006 This study clearly shows the route from ROS generation by 6-OHDA to initiation of p38/JNK signalling via activation of ASK1 in the studied PD model. Reactive Oxygen Species 40-43 mitogen-activated protein kinase 8 Homo sapiens 86-89 16540388-4 2006 In this review we will first summarize and discuss some recent findings regarding the signaling mechanisms of ROS-or RNS-mediated JNK activation. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 8 Homo sapiens 130-133 16540388-5 2006 Second, we will talk about the role of JNK in ROS-or RNS-mediated cell death (both apoptosis and necrosis). Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 39-42 16540388-7 2006 Taken together, the accumulating knowledge about the ROS/RNS-induced JNK signaling pathway has greatly advanced our understanding of the complex processes deciding the cellular responses to environmental stress. Reactive Oxygen Species 53-56 mitogen-activated protein kinase 8 Homo sapiens 69-72 16044154-8 2005 ROS accumulation was suppressed by the antioxidant butylated hydroxyanisol, which also abolished ATRA-induced JNK activation and apoptosis. Reactive Oxygen Species 0-3 mitogen-activated protein kinase 8 Homo sapiens 110-113 16412424-4 2006 Antioxidants and SP600125, an inhibitor of JNK1/2, but not inhibitors of p38 MAPK and MEK1/2, significantly prevented cell death, thus implying that reactive oxygen species and JNK1/2 play crucial roles in the CEP-induced apoptosis of HuH-7 cells. Reactive Oxygen Species 149-172 mitogen-activated protein kinase 8 Homo sapiens 43-49 16044154-9 2005 Altogether, our results demonstrate an anti-apoptotic effect of NF-kappaB activation during ATRA-induced differentiation of NB4 cells and identify repression of ROS-mediated JNK activation as a mechanism for this effect. Reactive Oxygen Species 161-164 mitogen-activated protein kinase 8 Homo sapiens 174-177 15940365-14 2005 CONCLUSIONS: Our data show that TNF-alpha increases intracellular ROS in hBMSC and that TNF-alpha and H2O2 induce apoptosis in hBMSC through the activation of JNK and NF-kappaB. Reactive Oxygen Species 66-69 mitogen-activated protein kinase 8 Homo sapiens 159-162 16278378-1 2005 PURPOSE AND EXPERIMENTAL DESIGN: Previously, we observed that the activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun NH(2)-terminal kinase (JNK1) is mediated through the activation of apoptosis signal-regulating kinase 1 (ASK1) as a result of the reactive oxygen species-mediated dissociation of glutaredoxin and thioredoxin from ASK1. Reactive Oxygen Species 264-287 mitogen-activated protein kinase 8 Homo sapiens 157-161 16151469-6 2005 The phospho-JNK inhibitor SP600125 partially protected Sup-M2 cells from LY293111-induced apoptosis, PARP cleavage and ROS generation, suggesting a role for JNK in LY293111-induced cell death. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 8 Homo sapiens 12-15 15755895-5 2005 Specific blockade of NF-kappaB in DCs induced strongly augmented JNK/AP-1 activity because of elevated levels of reactive oxygen species. Reactive Oxygen Species 113-136 mitogen-activated protein kinase 8 Homo sapiens 65-68 16149076-8 2005 It is thus conferred that such sequent events as ROS production, caspase activation, JNK/SAPK activation, bcl-2 phosphorylation and the further generation of ROS should be parts of an amplification loop to increase caspase activity, thereby facilitating the apoptotic cell death process. Reactive Oxygen Species 158-161 mitogen-activated protein kinase 8 Homo sapiens 85-88 15917192-10 2005 JNK-mediated apoptosis may limit damaging immune responses against neoepitopes generated by modification of self-antigens by reactive oxygen species present at sites of inflammation. Reactive Oxygen Species 125-148 mitogen-activated protein kinase 8 Homo sapiens 0-3 15705601-8 2005 To summarize, our studies suggest that EGCG induces stress signals by damaging mitochondria and ROS-mediated JNK activation in MIA PaCa-2 pancreatic carcinoma cells. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 8 Homo sapiens 109-112 15867371-7 2005 This process triggers a reactive oxygen species (ROS)-independent activation of the JNK-mediated pathway that results in a typical process of apoptosis. Reactive Oxygen Species 24-47 mitogen-activated protein kinase 8 Homo sapiens 84-87 15867371-7 2005 This process triggers a reactive oxygen species (ROS)-independent activation of the JNK-mediated pathway that results in a typical process of apoptosis. Reactive Oxygen Species 49-52 mitogen-activated protein kinase 8 Homo sapiens 84-87 15917192-0 2005 JNK activation limits dendritic cell maturation in response to reactive oxygen species by the induction of apoptosis. Reactive Oxygen Species 63-86 mitogen-activated protein kinase 8 Homo sapiens 0-3 15313424-1 2004 Reactive oxygen species (ROS), either directly or via the formation of lipid peroxidation products, such as 4-hydroxy-2-nonenal, acrolein and F2-isoprostanes, may play a role in enhancing inflammation through the activation and phosphorylation of stress kinases (JNK, ERK, p38) and redox-sensitive transcription factors such as NF-kappaB and AP-1. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 263-266 15701637-1 2005 The apoptosis signal-regulating kinase 1 (ASK1)-JNK/p38 signaling pathway is pivotal component in cell apoptosis and can be activated by a variety of death stimuli including tumor necrosis factor (TNF) alpha and oxidative stress (reactive oxygen species). Reactive Oxygen Species 230-253 mitogen-activated protein kinase 8 Homo sapiens 48-51 15809025-3 2005 Yet the mechanisms by which ROS trigger JNK signaling have remained elusive. Reactive Oxygen Species 28-31 mitogen-activated protein kinase 8 Homo sapiens 40-43 15592360-3 2005 We have reported that apoptosis signal-regulating kinase 1 (ASK1) is required for ROS- and ER stress-induced JNK activation and apoptosis. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 109-112 15604272-10 2004 Because it has been reported that reactive oxygen species are increased in hypoxia and related to JNK activation, we investigated their role in signaling this response. Reactive Oxygen Species 34-57 mitogen-activated protein kinase 8 Homo sapiens 98-101 15340045-8 2004 Moreover, Hep3B cells overexpressing JNK1 or stress-activated protein kinase kinase (SEK1) seem to be more susceptible to cell death from ROS and loss of DeltaPsim induced by VCA, whereas expression of dominant-negative JNK1 or SEK1 in Hep3B cells do not. Reactive Oxygen Species 138-141 mitogen-activated protein kinase 8 Homo sapiens 37-41 15537542-6 2004 FHC-mediated inhibition of JNK signaling depends on suppressing ROS accumulation and is achieved through iron sequestration. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 27-30 15537542-7 2004 These findings establish a basis for the NF-kappaB-mediated control of ROS induction and identify a mechanism by which NF-kappaB suppresses proapoptotic JNK signaling. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Homo sapiens 153-156 15352033-0 2004 Fenretinide induces sustained-activation of JNK/p38 MAPK and apoptosis in a reactive oxygen species-dependent manner in neuroblastoma cells. Reactive Oxygen Species 76-99 mitogen-activated protein kinase 8 Homo sapiens 44-47 15483317-5 2004 Upregulation of XIAP, A20 and blockers of reactive oxygen species (ROS) appear to be important additional means by which NF-kappaB blunts JNK signaling. Reactive Oxygen Species 42-65 mitogen-activated protein kinase 8 Homo sapiens 138-141 15483317-5 2004 Upregulation of XIAP, A20 and blockers of reactive oxygen species (ROS) appear to be important additional means by which NF-kappaB blunts JNK signaling. Reactive Oxygen Species 67-70 mitogen-activated protein kinase 8 Homo sapiens 138-141 15766528-0 2005 Reactive oxygen species promote TNFalpha-induced death and sustained JNK activation by inhibiting MAP kinase phosphatases. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 69-72 15766528-3 2005 Sustained JNK activation in NF-kappaB-deficient cells was suggested to depend on reactive oxygen species (ROS), but how ROS affect JNK activation was unclear. Reactive Oxygen Species 81-104 mitogen-activated protein kinase 8 Homo sapiens 10-13 15766528-3 2005 Sustained JNK activation in NF-kappaB-deficient cells was suggested to depend on reactive oxygen species (ROS), but how ROS affect JNK activation was unclear. Reactive Oxygen Species 106-109 mitogen-activated protein kinase 8 Homo sapiens 10-13 15766528-4 2005 We now show that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid. Reactive Oxygen Species 34-37 mitogen-activated protein kinase 8 Homo sapiens 145-148 15611622-5 2004 Moreover, NF-kappaB blunts accumulation of reactive oxygen species (ROS) induced by TNFalpha, and this antioxidant effect of NF-kappaB is also critical for inhibition of TNFalpha-induced JNK activation. Reactive Oxygen Species 43-66 mitogen-activated protein kinase 8 Homo sapiens 187-190 15611622-5 2004 Moreover, NF-kappaB blunts accumulation of reactive oxygen species (ROS) induced by TNFalpha, and this antioxidant effect of NF-kappaB is also critical for inhibition of TNFalpha-induced JNK activation. Reactive Oxygen Species 68-71 mitogen-activated protein kinase 8 Homo sapiens 187-190 15352033-8 2004 Our study demonstrates that in neuroblastoma cells, fenretinide induces sustained-activation of JNK and p38 MAPK in an ROS-dependent manner and indicates that JNK and p38 MAPK signaling might mediate fenretinide-induced apoptosis. Reactive Oxygen Species 119-122 mitogen-activated protein kinase 8 Homo sapiens 96-99 15313424-1 2004 Reactive oxygen species (ROS), either directly or via the formation of lipid peroxidation products, such as 4-hydroxy-2-nonenal, acrolein and F2-isoprostanes, may play a role in enhancing inflammation through the activation and phosphorylation of stress kinases (JNK, ERK, p38) and redox-sensitive transcription factors such as NF-kappaB and AP-1. Reactive Oxygen Species 25-28 mitogen-activated protein kinase 8 Homo sapiens 263-266 14716300-10 2004 In addition, JNK was activated by ASC upstream of mitochondria via reactive oxygen species. Reactive Oxygen Species 67-90 mitogen-activated protein kinase 8 Homo sapiens 13-16 15212948-0 2004 K(+) channel activity and redox status are differentially required for JNK activation by UV and reactive oxygen species. Reactive Oxygen Species 96-119 mitogen-activated protein kinase 8 Homo sapiens 71-74 15167449-14 2004 CONCLUSIONS: Ang II activates p38MAPK, JNK and ERK5 primarily through NAD(P)H oxidase-generated ROS. Reactive Oxygen Species 96-99 mitogen-activated protein kinase 8 Homo sapiens 39-42 15075471-2 2003 It was found that stimulation with cholecystokinin (CCK) or exposure of pancreatic acini to reactive oxygen species induces three separate signaling cascades leading to activation of ERKs, JNK/SAPKs and p38 MAPK. Reactive Oxygen Species 92-115 mitogen-activated protein kinase 8 Homo sapiens 189-192 12189133-3 2002 Apoptosis signal-regulating kinase (ASK) 1 is a MAP kinase kinase kinase that activates the JNK and p38 mitogen-activated protein (MAP) kinase cascades in response to environmental stresses such as reactive oxygen species. Reactive Oxygen Species 198-221 mitogen-activated protein kinase 8 Homo sapiens 92-95 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 8 Homo sapiens 75-83 14505349-6 2003 Collectively, our results demonstrate that Cur significantly attenuates UV irradiation-induced ROS formation, and suggest that ROS triggers JNK activation, which in turn causes MMP change, cytochrome C release, caspase activation, and subsequent apoptotic biochemical changes. Reactive Oxygen Species 127-130 mitogen-activated protein kinase 8 Homo sapiens 140-143 12898340-4 2003 The results showed that the signal transduction pathway of MPP+-induced apoptosis might be ROS to JNK, then to caspase-3. Reactive Oxygen Species 91-94 mitogen-activated protein kinase 8 Homo sapiens 98-101 12898340-8 2003 The removal of ROS might inhibit the activity of JNK and the expression of cleaved caspase-3. Reactive Oxygen Species 15-18 mitogen-activated protein kinase 8 Homo sapiens 49-52 11313966-2 2001 However, the exact mechanisms by which reactive oxygen species (ROS) activate JNK are unclear. Reactive Oxygen Species 39-62 mitogen-activated protein kinase 8 Homo sapiens 78-81 12361705-0 2002 Reactive oxygen species stimulated human hepatoma cell proliferation via cross-talk between PI3-K/PKB and JNK signaling pathways. Reactive Oxygen Species 0-23 mitogen-activated protein kinase 8 Homo sapiens 106-109 12361705-13 2002 Taken together, we found that ROS regulate hepatoma cell growth via specific signaling pathways (cross-talk between PI3-K/PKB and JNK pathway) which may provide a novel clue to elucidate the mechanism of hepatoma carcinogenesis. Reactive Oxygen Species 30-33 mitogen-activated protein kinase 8 Homo sapiens 130-133 11279018-4 2001 Raising intracellular ROS by depletion of glutathione with buthionine sulfoximine (BSO) or glutamine starvation resulted in down-regulation of Pgp and p27Kip1, whereas ERK1,2 and JNK were activated. Reactive Oxygen Species 22-25 mitogen-activated protein kinase 8 Homo sapiens 179-182 11313966-2 2001 However, the exact mechanisms by which reactive oxygen species (ROS) activate JNK are unclear. Reactive Oxygen Species 64-67 mitogen-activated protein kinase 8 Homo sapiens 78-81 10970698-3 2000 We extend these findings and show that the stimulation of JNK and apoptosis by antagonist G is dependent upon the generation of reactive oxygen species (ROS) being inhibited either by anoxia or the presence of N-acetyl cysteine (n-AC). Reactive Oxygen Species 128-151 mitogen-activated protein kinase 8 Homo sapiens 58-61 10970698-3 2000 We extend these findings and show that the stimulation of JNK and apoptosis by antagonist G is dependent upon the generation of reactive oxygen species (ROS) being inhibited either by anoxia or the presence of N-acetyl cysteine (n-AC). Reactive Oxygen Species 153-156 mitogen-activated protein kinase 8 Homo sapiens 58-61 9927052-9 1999 These results confirm again that ROS acts as a mediator for JNK activation during beta-Lap-induced apoptosis. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 60-63 10840014-13 2000 CONCLUSIONS: The present study indicates that reactive oxygen species induced by high glucose may be involved in JNK activation, which in turn triggers the caspase-3 that facilitates the apoptosis in HUVECs. Reactive Oxygen Species 46-69 mitogen-activated protein kinase 8 Homo sapiens 113-116 10837498-7 2000 That ROS acted as a key intermediate in the CHG pathway was supported by the following evidence: 1) increased superoxide levels similar to those observed with PMA or TNFalpha, 2) increased phosphorylation of stress-responsive mitogen-activated protein kinases p38 and JNK-1, 3) counteraction of the effects of CHG on TNFalpha production, the 295TNFluc reporter activity, activation of NF-kappaB, and repression of IkappaBalpha by antioxidants and p38 mitogen-activated protein kinase inhibitors. Reactive Oxygen Species 5-8 mitogen-activated protein kinase 8 Homo sapiens 268-273 10748578-5 1999 The JNK and AP-1 activation is mediated with radiation-released free radicals in ROS 17/2.8 osteoblasts. Reactive Oxygen Species 81-84 mitogen-activated protein kinase 8 Homo sapiens 4-7 10748578-6 1999 These results indicate that ionizing radiation at a single dose of up to 5 Gray stimulates differentiation of ROS 17/2.8 osteoblasts via free radial release which may affect JNK/SAPK and AP-1 activities. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 8 Homo sapiens 174-182 9452508-7 1998 Anti-oxidants N-acetylcysteine and catalase, which serve as scavengers of reactive oxygen species generated by metabolic DA oxidation, effectively block DA-induced JNK activation and subsequent apoptosis. Reactive Oxygen Species 74-97 mitogen-activated protein kinase 8 Homo sapiens 164-167 33806765-8 2021 Taken together, these findings indicated that the hypoxia-induced atrial profibrotic response occurs mainly via the ROS/JNK pathway, its downstream upregulation of HIF-1alpha and c-Jun/ATF2 phosphorylation and nuclear translocation to up-regulate the expression of fibrosis-related proteins (COL1A, COL3A, TGF-beta1 and alpha-SMA). Reactive Oxygen Species 116-119 mitogen-activated protein kinase 8 Homo sapiens 120-123 33778293-0 2021 Power of an Organic Electron Acceptor in Modulation of Intracellular Mitochondrial Reactive Oxygen Species: Inducing JNK- and Caspase-Dependent Apoptosis of Cancer Cells. Reactive Oxygen Species 83-106 mitogen-activated protein kinase 8 Homo sapiens 117-120 33778293-5 2021 This effect of BBT in ROS generation activates JNK and p38 stress-dependent pathways and resulted in mitochondrial-dependent apoptotic cell death with the reduction in expression of several important cyto-protecting factors (Hsp27 and NFkappaB), indicating its potential in inhibition of cancer cell relapse. Reactive Oxygen Species 22-25 mitogen-activated protein kinase 8 Homo sapiens 47-50 33803748-9 2021 c-Jun N-terminal kinase 1 (JNK1) and p53 as downstream mediators of oxidative stress contributed to the synergistic toxicity by co-exposure of patulin and cadmium, while p53/JNK1 activation promoted the second-round ROS production through a positive feedback loop. Reactive Oxygen Species 216-219 mitogen-activated protein kinase 8 Homo sapiens 0-25 33803748-9 2021 c-Jun N-terminal kinase 1 (JNK1) and p53 as downstream mediators of oxidative stress contributed to the synergistic toxicity by co-exposure of patulin and cadmium, while p53/JNK1 activation promoted the second-round ROS production through a positive feedback loop. Reactive Oxygen Species 216-219 mitogen-activated protein kinase 8 Homo sapiens 27-31 33806765-9 2021 Our result suggests that suppression of ROS/JNK signaling pathway is a critical mechanism for developing a novel therapeutic strategy against atrial fibrillation. Reactive Oxygen Species 40-43 mitogen-activated protein kinase 8 Homo sapiens 44-47 33589596-10 2021 NAC, a reactive oxygen species (ROS) inhibitor, reduces GSDME cleavage through JNK signaling in human renal tubular epithelial cells. Reactive Oxygen Species 32-35 mitogen-activated protein kinase 8 Homo sapiens 79-82 33589596-11 2021 Thus, we speculate that renal tubular epithelial cell pyroptosis induced by chemotherapy drugs is mediated by ROS-JNK-caspase 3-GSDME signaling, implying that therapies targeting GSDME may prove efficacious in overcoming chemotherapeutic drug-induced nephrotoxicity. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 8 Homo sapiens 114-117 34763314-0 2022 The new andrographolide derivative AGS-30 induces apoptosis in human colon cancer cells by activating a ROS-dependent JNK signalling pathway. Reactive Oxygen Species 104-107 mitogen-activated protein kinase 8 Homo sapiens 118-121 34826531-6 2022 Meanwhile, Au NS exhibited enhanced ROS scavenging efficiency of hydrogen peroxides and superoxide, which was helpful to restrain the activity of peroxisome proliferators-activated receptors beta (PPARbeta) and c-Jun N-terminal kinase (JNK), thereby reducing HSCs proliferation to enhance HSCs inactivation efficacy. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 211-234 34826531-6 2022 Meanwhile, Au NS exhibited enhanced ROS scavenging efficiency of hydrogen peroxides and superoxide, which was helpful to restrain the activity of peroxisome proliferators-activated receptors beta (PPARbeta) and c-Jun N-terminal kinase (JNK), thereby reducing HSCs proliferation to enhance HSCs inactivation efficacy. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 236-239 34763314-11 2022 Moreover, these elevated levels of the proteins were inhibited by the antioxidant N-acetylcysteine and the JNK inhibitor SP600125, suggesting the involvement of ROS/JNK-dependent mechanisms in AGS-30-induced apoptosis. Reactive Oxygen Species 161-164 mitogen-activated protein kinase 8 Homo sapiens 107-110 34763314-11 2022 Moreover, these elevated levels of the proteins were inhibited by the antioxidant N-acetylcysteine and the JNK inhibitor SP600125, suggesting the involvement of ROS/JNK-dependent mechanisms in AGS-30-induced apoptosis. Reactive Oxygen Species 161-164 mitogen-activated protein kinase 8 Homo sapiens 165-168 34763314-14 2022 AGS-30 induces apoptosis of colon cancer cells through ROS/JNK-dependent pathway. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 8 Homo sapiens 59-62 34369083-4 2021 Mechanistically, co-targeting FGFR1 and PLK1 upregulates reactive oxygen species (ROS), leading to oxidative stress-activated c-Jun N-terminal kinase (JNK)/p38 pathway and E2F1-induced apoptosis. Reactive Oxygen Species 57-80 mitogen-activated protein kinase 8 Homo sapiens 126-149 34481340-13 2021 Treatment with the ROS scavenger N-acetyl cysteine, effectively reversed the induction of apoptosis, autophagy, JNK activation and DNA damage elicited by RA. Reactive Oxygen Species 19-22 mitogen-activated protein kinase 8 Homo sapiens 112-115 34776955-5 2021 This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation. Reactive Oxygen Species 124-127 mitogen-activated protein kinase 8 Homo sapiens 218-221 34280394-8 2021 Hepatic injury may be aggravated by ROS, which induce oxidative stress and the phosphorylation of p38 mitogen-activated protein kinase, Jun N-terminal kinase, extracellular regulated protein kinase, signal transducer and activator of transcription 3 and nuclear factor kappa-B. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 136-157 34468764-0 2021 Magnesium isoglycyrrhizinate prevents cadmium-induced activation of JNK and apoptotic hepatocyte death by reversing ROS-inactivated PP2A. Reactive Oxygen Species 116-119 mitogen-activated protein kinase 8 Homo sapiens 68-71 34468764-11 2021 Eliminating ROS by N-acetyl-l-cysteine abrogated Cd-induced PP2A-JNK pathway disruption and concurrently reinforced MgIG-conferred protective effects, which could be further slightly strengthened by PP2A overexpression. Reactive Oxygen Species 12-15 mitogen-activated protein kinase 8 Homo sapiens 65-68 34494324-4 2021 The molecular mechanism of inhibiting cell migration and EMT processes may be related to the inhibition of SIRT1, and the mechanism of apoptosis induction is associated with the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) pathway-mediated activation of mitochondrial apoptotic pathway. Reactive Oxygen Species 178-201 mitogen-activated protein kinase 8 Homo sapiens 233-236 34494324-4 2021 The molecular mechanism of inhibiting cell migration and EMT processes may be related to the inhibition of SIRT1, and the mechanism of apoptosis induction is associated with the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) pathway-mediated activation of mitochondrial apoptotic pathway. Reactive Oxygen Species 203-206 mitogen-activated protein kinase 8 Homo sapiens 233-236 34834209-0 2021 Regulation of ROS-Dependent JNK Pathway by 2"-Hydroxycinnamaldehyde Inducing Apoptosis in Human Promyelocytic HL-60 Leukemia Cells. Reactive Oxygen Species 14-17 mitogen-activated protein kinase 8 Homo sapiens 28-31 34834209-7 2021 Taken together, our findings suggest that 2"-HCA induces apoptosis via the ROS-dependent JNK pathway and could be considered as a potential therapeutic agent for leukemia. Reactive Oxygen Species 75-78 mitogen-activated protein kinase 8 Homo sapiens 89-92 34683920-0 2021 Induction of Apoptosis by Isoalantolactone in Human Hepatocellular Carcinoma Hep3B Cells through Activation of the ROS-Dependent JNK Signaling Pathway. Reactive Oxygen Species 115-118 mitogen-activated protein kinase 8 Homo sapiens 129-132 34683920-8 2021 IALT also improved the generation of intracellular reactive oxygen species (ROS), whereas the ROS inhibitor significantly abrogated IALT-induced growth reduction, apoptosis, and JNK activation. Reactive Oxygen Species 94-97 mitogen-activated protein kinase 8 Homo sapiens 178-181 34683920-10 2021 Taken together, our findings indicate that IALT exhibited anti-cancer activity in HCC Hep3B cells by inducing ROS-dependent activation of the JNK signaling pathway. Reactive Oxygen Species 110-113 mitogen-activated protein kinase 8 Homo sapiens 142-145 34369083-4 2021 Mechanistically, co-targeting FGFR1 and PLK1 upregulates reactive oxygen species (ROS), leading to oxidative stress-activated c-Jun N-terminal kinase (JNK)/p38 pathway and E2F1-induced apoptosis. Reactive Oxygen Species 57-80 mitogen-activated protein kinase 8 Homo sapiens 151-154 34369083-4 2021 Mechanistically, co-targeting FGFR1 and PLK1 upregulates reactive oxygen species (ROS), leading to oxidative stress-activated c-Jun N-terminal kinase (JNK)/p38 pathway and E2F1-induced apoptosis. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 126-149 34369083-4 2021 Mechanistically, co-targeting FGFR1 and PLK1 upregulates reactive oxygen species (ROS), leading to oxidative stress-activated c-Jun N-terminal kinase (JNK)/p38 pathway and E2F1-induced apoptosis. Reactive Oxygen Species 82-85 mitogen-activated protein kinase 8 Homo sapiens 151-154 34305590-8 2021 Moreover, triclabendazole induced reactive oxygen species (ROS) elevation and increased JNK phosphorylation and lytic cell death, which could be rescued by the ROS scavenger (NAC), suggesting that triclabendazole-induced GSDME-dependent pyroptosis is related to the ROS/JNK/Bax-mitochondrial apoptotic pathway. Reactive Oxygen Species 160-163 mitogen-activated protein kinase 8 Homo sapiens 88-91 34578957-5 2021 Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-Jun N-terminal kinase (JNK) induced by TPA. Reactive Oxygen Species 55-78 mitogen-activated protein kinase 8 Homo sapiens 124-147 34578957-5 2021 Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-Jun N-terminal kinase (JNK) induced by TPA. Reactive Oxygen Species 55-78 mitogen-activated protein kinase 8 Homo sapiens 149-152 34578957-5 2021 Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-Jun N-terminal kinase (JNK) induced by TPA. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 8 Homo sapiens 124-147 34578957-5 2021 Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-Jun N-terminal kinase (JNK) induced by TPA. Reactive Oxygen Species 80-83 mitogen-activated protein kinase 8 Homo sapiens 149-152 34242793-4 2021 Mechanistically, this protective autophagy is regulated by intracellular reactive oxygen species (ROS) accumulation, which triggers the downstream signals of JNK, Bcl-2 and Beclin-1. Reactive Oxygen Species 73-96 mitogen-activated protein kinase 8 Homo sapiens 158-161 34242793-4 2021 Mechanistically, this protective autophagy is regulated by intracellular reactive oxygen species (ROS) accumulation, which triggers the downstream signals of JNK, Bcl-2 and Beclin-1. Reactive Oxygen Species 98-101 mitogen-activated protein kinase 8 Homo sapiens 158-161 34242793-5 2021 More importantly, soft substrate-induced activation of ROS/JNK signaling promotes cell apoptosis through the mitochondrial pathway, whereas it increases protective autophagy by suppressing the interaction of Bcl-2 and Beclin-1. Reactive Oxygen Species 55-58 mitogen-activated protein kinase 8 Homo sapiens 59-62 34413791-4 2021 The activation of JNK under hypoxic conditions was dependent on overproduction of mitochondrial reactive oxygen species (mtROS) in cardiomyocytes, and mitochondrial division was identified as the upstream inducer of mtROS overproduction. Reactive Oxygen Species 96-119 mitogen-activated protein kinase 8 Homo sapiens 18-21 34367464-0 2021 Advanced Oxidation Protein Products Induce G1/G0-Phase Arrest in Ovarian Granulosa Cells via the ROS-JNK/p38 MAPK-p21 Pathway in Premature Ovarian Insufficiency. Reactive Oxygen Species 97-100 mitogen-activated protein kinase 8 Homo sapiens 101-104 34214663-6 2021 By RNA sequencing technique, the result was ascribed to the reactive oxygen species (ROS) mediated TNF-JNK pathway and cell cycle arrest besides breaking DNA, in contrast to only DNA damage only with those untargeted nanoparticles. Reactive Oxygen Species 60-83 mitogen-activated protein kinase 8 Homo sapiens 103-106 34214663-6 2021 By RNA sequencing technique, the result was ascribed to the reactive oxygen species (ROS) mediated TNF-JNK pathway and cell cycle arrest besides breaking DNA, in contrast to only DNA damage only with those untargeted nanoparticles. Reactive Oxygen Species 85-88 mitogen-activated protein kinase 8 Homo sapiens 103-106 34475984-5 2021 The inhibition of ROS generation by N-acetyl-l-cysteine not only recovered cell migration and viability, but also reduced beta-catenin accumulation and JNK and ERK activation. Reactive Oxygen Species 18-21 mitogen-activated protein kinase 8 Homo sapiens 152-155 34290233-9 2021 We also demonstrated that GSTA2 played crucial roles in regulating the ROS-associated JNK and AKT signaling pathways and ROS metabolism in HCCs in responding to a dynamic ROS environment. Reactive Oxygen Species 71-74 mitogen-activated protein kinase 8 Homo sapiens 86-89 34290233-9 2021 We also demonstrated that GSTA2 played crucial roles in regulating the ROS-associated JNK and AKT signaling pathways and ROS metabolism in HCCs in responding to a dynamic ROS environment. Reactive Oxygen Species 171-174 mitogen-activated protein kinase 8 Homo sapiens 86-89 35571453-12 2022 Conclusions: The results suggest that BBR induces apoptosis of NSCLC cells via ROS-mediated ASK1/JNK activation and the mitochondrial pathway. Reactive Oxygen Species 79-82 mitogen-activated protein kinase 8 Homo sapiens 97-100 34107857-8 2021 Subsequently, the activation of the ROS/JNK signaling pathway was investigated. Reactive Oxygen Species 36-39 mitogen-activated protein kinase 8 Homo sapiens 40-43 35259676-0 2022 Punicalagin promotes autophagic degradation of human papillomavirus E6 and E7 proteins in cervical cancer through the ROS-JNK-BCL2 pathway. Reactive Oxygen Species 118-121 mitogen-activated protein kinase 8 Homo sapiens 122-125 35259676-5 2022 Additionally, punicalagin activated the reactive oxygen species (ROS)-JNK pathway and promoted the phosphorylation of BCL2, which led to the dissociation of BCL2 from BECN1 and the induction of autophagy. Reactive Oxygen Species 40-63 mitogen-activated protein kinase 8 Homo sapiens 70-73 35259676-5 2022 Additionally, punicalagin activated the reactive oxygen species (ROS)-JNK pathway and promoted the phosphorylation of BCL2, which led to the dissociation of BCL2 from BECN1 and the induction of autophagy. Reactive Oxygen Species 65-68 mitogen-activated protein kinase 8 Homo sapiens 70-73 35427423-4 2022 Mechanistic studies showed that inhibition of the JNK pathway upregulated the expression of quiescence-associated and stemness genes in HSCs, preventing HSCs from entering the cell cycle, increasing glucose uptake and accumulating reactive oxygen species (ROS). Reactive Oxygen Species 231-254 mitogen-activated protein kinase 8 Homo sapiens 50-53 35427423-4 2022 Mechanistic studies showed that inhibition of the JNK pathway upregulated the expression of quiescence-associated and stemness genes in HSCs, preventing HSCs from entering the cell cycle, increasing glucose uptake and accumulating reactive oxygen species (ROS). Reactive Oxygen Species 256-259 mitogen-activated protein kinase 8 Homo sapiens 50-53 35571453-0 2022 Berberine induces non-small cell lung cancer apoptosis via the activation of the ROS/ASK1/JNK pathway. Reactive Oxygen Species 81-84 mitogen-activated protein kinase 8 Homo sapiens 90-93 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Reactive Oxygen Species 230-233 mitogen-activated protein kinase 8 Homo sapiens 99-115 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Reactive Oxygen Species 230-233 mitogen-activated protein kinase 8 Homo sapiens 117-120 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Reactive Oxygen Species 230-233 mitogen-activated protein kinase 8 Homo sapiens 130-133 35315184-7 2022 PSO treatment rapidly boosts the ROS generation, which is responsible for the PSO-triggered DNA damage, mitochondria membrane potential decrease and caspase 3/7 activation, and c-Jun N-terminal kinase 1/2 activation. Reactive Oxygen Species 33-36 mitogen-activated protein kinase 8 Homo sapiens 177-204 35359571-7 2022 Together, D-JNKI-1 plays an essential role in protecting against neomycin-induced HEI-OC1 cell apoptosis by suppressing ROS generation, which inhibited JNK activation and AMPK and p38 phosphorylation to ameliorate JNK-mediated HEI-OC1 cell apoptosis. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 152-155 35359571-7 2022 Together, D-JNKI-1 plays an essential role in protecting against neomycin-induced HEI-OC1 cell apoptosis by suppressing ROS generation, which inhibited JNK activation and AMPK and p38 phosphorylation to ameliorate JNK-mediated HEI-OC1 cell apoptosis. Reactive Oxygen Species 120-123 mitogen-activated protein kinase 8 Homo sapiens 214-217 35044214-1 2022 We previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Reactive Oxygen Species 76-99 mitogen-activated protein kinase 8 Homo sapiens 131-134 35044214-1 2022 We previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Reactive Oxygen Species 101-104 mitogen-activated protein kinase 8 Homo sapiens 131-134 35044214-12 2022 IMPORTANCE ROS/JNK signaling pathway contributes to liver diseases, including steatosis, metabolic disorders, and hepatocellular carcinoma. Reactive Oxygen Species 11-14 mitogen-activated protein kinase 8 Homo sapiens 15-18 35044214-13 2022 We previously reported that HCV activates the ROS/JNK signaling pathway, leading to the enhancement of hepatic gluconeogenesis and apoptosis induction. Reactive Oxygen Species 46-49 mitogen-activated protein kinase 8 Homo sapiens 50-53 35044214-15 2022 We provide evidence suggesting that HCV infection promotes the ROS/JNK/Itch signaling pathway and ESCRT/VPS4A machinery to release infectious HCV particles. Reactive Oxygen Species 63-66 mitogen-activated protein kinase 8 Homo sapiens 67-70