PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32956685-0 2020 Resveratrol protects retinal ganglion cell axons through regulation of the SIRT1-JNK pathway. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 81-84 32956685-5 2020 Resveratrol increased the expression of SIRT1 while decreasing the phosphorylation of N-terminal kinase (JNK). Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 105-108 32956685-7 2020 Simultaneous administration of resveratrol and sirtinol (SIRT1 inhibitor) neither increased the expression of SIRT1 nor decreased the phosphorylation of JNK, indicating that resveratrol affects the phosphorylation of JNK by SIRT1. Resveratrol 174-185 mitogen-activated protein kinase 8 Homo sapiens 217-220 32956685-8 2020 In total, our research shows that resveratrol treatment significantly reduces apoptosis and axonal degeneration of RGCs, and this protection is partly mediated through the SIRT1-JNK pathway. Resveratrol 34-45 mitogen-activated protein kinase 8 Homo sapiens 178-181 30537632-8 2019 Resveratrol limited the activation of TAK1 and its downstream signaling pathway, including the degradation of IkappaBalpha, the activation of NF-kappaB P65 and the phosphorylation of P38 and JNK. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 191-194 31499271-6 2019 Further study revealed that resveratrol could increase the protein levels of TLR4, Ikk, IkappaBalpha, NF-kappaB and JNK when compared with non-adjuvant group. Resveratrol 28-39 mitogen-activated protein kinase 8 Homo sapiens 116-119 30384152-0 2019 Resveratrol represses tumor necrosis factor alpha/c-Jun N-terminal kinase signaling via autophagy in human dental pulp stem cells. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 50-73 30384152-8 2019 In contrast, resveratrol dramatically inhibited TNFalpha-induced phosphorylation of c-Jun N-terminal kinase (JNK) MAPK. Resveratrol 13-24 mitogen-activated protein kinase 8 Homo sapiens 84-107 30384152-12 2019 CONCLUSIONS: The results suggest that resveratrol suppresses TNFalpha-induced inflammatory cytokines expressed by DPSCs through regulating the inhibitory autophagy-JNK signaling cascade. Resveratrol 38-49 mitogen-activated protein kinase 8 Homo sapiens 164-167 30384152-8 2019 In contrast, resveratrol dramatically inhibited TNFalpha-induced phosphorylation of c-Jun N-terminal kinase (JNK) MAPK. Resveratrol 13-24 mitogen-activated protein kinase 8 Homo sapiens 109-112 28590410-7 2017 Furthermore, the effect of resveratrol on the levels of MITF and tyrosinase was suppressed when melanocytes were pre-treated with SP600125 (JNK inhibitor). Resveratrol 27-38 mitogen-activated protein kinase 8 Homo sapiens 140-143 25401496-10 2015 CONCLUSION: In summary, resveratrol inhibited MMP-9 expression and oral cancer cell metastasis by downregulating JNK1/2 and ERK1/2 signals pathways and, thus, exerts beneficial effects in chemoprevention. Resveratrol 24-35 mitogen-activated protein kinase 8 Homo sapiens 113-119 26146868-0 2015 Resveratrol prevents cadmium activation of Erk1/2 and JNK pathways from neuronal cell death via protein phosphatases 2A and 5. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 54-57 26146868-7 2015 Over-expression of PP2A or PP5 strengthened the inhibitory effects of resveratrol on Cd-induced activation of Erk1/2 and/or JNK, as well as cell death. Resveratrol 70-81 mitogen-activated protein kinase 8 Homo sapiens 124-127 26146868-8 2015 The results indicate that resveratrol prevents Cd-induced activation of Erk1/2 and JNK pathways and neuronal cell death in part via activating PP2A and PP5. Resveratrol 26-37 mitogen-activated protein kinase 8 Homo sapiens 83-86 25619392-0 2015 Resveratrol induces apoptosis of human chronic myelogenous leukemia cells in vitro through p38 and JNK-regulated H2AX phosphorylation. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 99-102 26124921-4 2015 Resveratrol transiently induced Egr-1 through ERK/JNK-ElK-1. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 50-53 25619392-8 2015 Pretreatment with the p38 inhibitor SB202190 or the JNK inhibitor SP600125 dose-dependently reduced resveratrol-induced phosphorylation of H2AX, which were also observed when the cells were transfected with p38- or JNK-specific siRNAs. Resveratrol 100-111 mitogen-activated protein kinase 8 Homo sapiens 215-218 25619392-11 2015 CONCLUSION: H2AX phosphorylation at Ser139 in human CML cells, which is regulated by p38 and JNK, is essential for resveratrol-induced apoptosis. Resveratrol 115-126 mitogen-activated protein kinase 8 Homo sapiens 93-96 25619392-7 2015 Resveratrol treatment activated two MAPK family members p38 and JNK, and blocked the activation of another MAPK family member ERK. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 64-67 25619392-8 2015 Pretreatment with the p38 inhibitor SB202190 or the JNK inhibitor SP600125 dose-dependently reduced resveratrol-induced phosphorylation of H2AX, which were also observed when the cells were transfected with p38- or JNK-specific siRNAs. Resveratrol 100-111 mitogen-activated protein kinase 8 Homo sapiens 52-55 24841706-7 2014 Treatment with SP600125, a JNK inhibitor, attenuated the effects of resveratrol on MMP-2 and MMP-9, and accelerated resveratrol-induced effects on type II collagen, SOX-9 and sulfated proteoglycan production. Resveratrol 68-79 mitogen-activated protein kinase 8 Homo sapiens 27-30 24841706-0 2014 Resveratrol attenuates matrix metalloproteinase-9 and -2-regulated differentiation of HTB94 chondrosarcoma cells through the p38 kinase and JNK pathways. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 140-143 24841706-5 2014 Phosphorylation of p38 was increased and phosphorylation of c-Jun N-terminal kinase (JNK) was inhibited by resveratrol. Resveratrol 107-118 mitogen-activated protein kinase 8 Homo sapiens 60-83 24841706-5 2014 Phosphorylation of p38 was increased and phosphorylation of c-Jun N-terminal kinase (JNK) was inhibited by resveratrol. Resveratrol 107-118 mitogen-activated protein kinase 8 Homo sapiens 85-88 24841706-8 2014 Our results suggest that resveratrol inhibits MMP-induced differentiation via the p38 kinase and JNK pathways in HTB94 chondrosarcoma cells. Resveratrol 25-36 mitogen-activated protein kinase 8 Homo sapiens 97-100 23437203-6 2013 Western blot analysis also showed that resveratrol inhibits phosphorylation of JNK1/2. Resveratrol 39-50 mitogen-activated protein kinase 8 Homo sapiens 79-85 24971582-9 2014 Furthermore, resveratrol (10 muM) attenuated HG-induced phosphorylation of Akt, p38 mitogen-activated protein kinase (MAPK), ERK 1/2, and JNK1/2 without affecting total levels. Resveratrol 13-24 mitogen-activated protein kinase 8 Homo sapiens 138-144 24971582-11 2014 CONCLUSIONS: Resveratrol inhibits HG-induced oxidative stress and VSMC proliferation by suppressing ROS generation, NADPH oxidase, Akt phosphorylation, p38 MAPK/JNK/ERK phosphorylation, and IkappaB-alpha and NF-kappaB activities. Resveratrol 13-24 mitogen-activated protein kinase 8 Homo sapiens 161-164 23199342-8 2013 Resveratrol and Ad-SIRT1 inhibited nicotine and LPS-mediated protein kinase C (PKC), phosphatidylinositol 3-kinase (PI3K), p38, ERK, JNK, MAPK and nuclear factor-kappa B (NF-kappaB) activation. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 133-136 22925919-6 2013 We found that resveratrol diminishes the effect of LPS on TRAF6 ubiquitination and activation of JNK and p38 MAP kinases, while it has no effect on the activation of extracellular-signal-regulated kinase (ERK)1/2. Resveratrol 14-25 mitogen-activated protein kinase 8 Homo sapiens 97-100 22925919-7 2013 The effect of resveratrol on MAP kinase inhibition is significant since TRAF6 activation was reported to induce activation of JNK and p38 MAP kinase while not affecting ERK1/2. Resveratrol 14-25 mitogen-activated protein kinase 8 Homo sapiens 126-129 18222423-4 2008 Our observations indicated that resveratrol, a polyphenolic phytoalexin, decreased STAT3 and NF-kappaB activation, while activating JNK-cJun that finally suppressed expression of cFLIP and Bcl-xL proteins and increased sensitivity to exogenous TRAIL in DR5-positive melanomas. Resveratrol 32-43 mitogen-activated protein kinase 8 Homo sapiens 132-135 23137540-6 2012 Conversely, suppression of SIRT1 activity with nicotinamide inhibited the effect of resveratrol on JNK phosphorylation, leading to restoration of resistance to oxidation-induced apoptosis. Resveratrol 84-95 mitogen-activated protein kinase 8 Homo sapiens 99-102 20082299-6 2010 Resveratrol-enhanced perforin expression and cytotoxic activity are effectively inhibited by pretreatment with the inhibitors of JNK (SP600125), ERK-1/2 (PD98059), or by siRNAs against JNK-1 and ERK-2. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 129-132 20082299-6 2010 Resveratrol-enhanced perforin expression and cytotoxic activity are effectively inhibited by pretreatment with the inhibitors of JNK (SP600125), ERK-1/2 (PD98059), or by siRNAs against JNK-1 and ERK-2. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 185-190 20082299-11 2010 Data presented strongly indicate that resveratrol act via NKG2D-dependent JNK and ERK-1/2 pathways. Resveratrol 38-49 mitogen-activated protein kinase 8 Homo sapiens 74-77 20103647-0 2010 Resveratrol promotes autophagic cell death in chronic myelogenous leukemia cells via JNK-mediated p62/SQSTM1 expression and AMPK activation. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 85-88 20103647-3 2010 Here, we report that the plant phytoalexin resveratrol (RSV) triggers autophagy in imatinib-sensitive and imatinib-resistant chronic myelogenous leukemia (CML) cells via JNK-dependent accumulation of p62. Resveratrol 43-54 mitogen-activated protein kinase 8 Homo sapiens 170-173 20103647-3 2010 Here, we report that the plant phytoalexin resveratrol (RSV) triggers autophagy in imatinib-sensitive and imatinib-resistant chronic myelogenous leukemia (CML) cells via JNK-dependent accumulation of p62. Resveratrol 56-59 mitogen-activated protein kinase 8 Homo sapiens 170-173 20103647-4 2010 JNK inhibition or p62 knockdown prevented RSV-mediated autophagy and antileukemic effects. Resveratrol 42-45 mitogen-activated protein kinase 8 Homo sapiens 0-3 20103647-8 2010 We concluded that RSV triggered autophagic cell death in CML cells via both JNK-mediated p62 overexpression and AMPK activation. Resveratrol 18-21 mitogen-activated protein kinase 8 Homo sapiens 76-79 20111678-5 2009 Resveratrol inhibited CTN-induced ROS generation, activation of JNK, loss of mitochondrial membrane potential (MMP), as well as activation of caspase-9, caspase-3 and PAK2. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 64-67 18776171-4 2009 In addition, RSV attenuated 10,12 CLA increase of intracellular calcium and reactive oxygen species associated with cellular stress, and activation of stress-related proteins (i.e., activating transcription factor 3, JNK) within 12 h. 10,12 CLA-mediated insulin resistance and suppression of fatty acid uptake and triglyceride content were attenuated by RSV. Resveratrol 13-16 mitogen-activated protein kinase 8 Homo sapiens 217-220 23137540-5 2012 Furthermore, ectopic expression of SIRT1 and treatment with resveratrol (a SIRT1 activator) attenuated JNK phosphorylation, which is a prerequisite for resistance to oxidative stress-induced apoptosis. Resveratrol 60-71 mitogen-activated protein kinase 8 Homo sapiens 103-106 20458181-3 2010 Our recent data reveals that RSV triggered autophagic cell death (ACD) in Chronic Myelogenous Leukemia (CML) cells, via both AMPK activation and JNK-mediated p62/SQSTM1 expression. Resveratrol 29-32 mitogen-activated protein kinase 8 Homo sapiens 145-148 20458181-4 2010 Here we discuss how Resveratrol can mediate ACD in CML cells and the possibility of utilizing the AMPK/mTOR and JNK/p62 pathways via Resveratrol to combat CML and other hematopoietic malignancies. Resveratrol 133-144 mitogen-activated protein kinase 8 Homo sapiens 112-115 20111678-9 2009 These results collectively demonstrate that CTN stimulates ROS generation and JNK activation for mitochondria-dependent apoptotic signaling in Hep G2 cells, and these apoptotic biochemical events are blocked by pretreatment with resveratrol, which exerts antioxidant effects. Resveratrol 229-240 mitogen-activated protein kinase 8 Homo sapiens 78-81 16322078-0 2006 Resveratrol protects against 4-hydroxynonenal-induced apoptosis by blocking JNK and c-JUN/AP-1 signaling. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 76-79 20641411-8 2004 Several research studies have reported that resveratrol has the ability to induce p53-dependent apoptosis in several cancer cell lines, and that the signal transduction pathways implicated in resveratrol action includes those of extracellular-regulated kinases 1 and 2 (ERK1/2), p38 kinase, and Jun N-terminal kinase (JNK) (6, 7). Resveratrol 192-203 mitogen-activated protein kinase 8 Homo sapiens 295-316 20641411-8 2004 Several research studies have reported that resveratrol has the ability to induce p53-dependent apoptosis in several cancer cell lines, and that the signal transduction pathways implicated in resveratrol action includes those of extracellular-regulated kinases 1 and 2 (ERK1/2), p38 kinase, and Jun N-terminal kinase (JNK) (6, 7). Resveratrol 192-203 mitogen-activated protein kinase 8 Homo sapiens 318-321 17049495-4 2007 Resveratrol-induced CHOP mRNA (and also protein) expression was inhibited by JNK specific inhibitor, but not ERK, p38 MAPK, PI3K and NF-kappaB inhibitors. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 77-80 16322078-4 2006 Resveratrol effectively prevented HNE-induced JNK and caspase activation, and hence apoptosis. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 46-49 16322078-8 2006 In light of the JNK-dependent induction of c-Jun/AP-1 activation and the protective role of resveratrol, these data may show a critical potential role for JNK in the cellular response against toxic products of lipid peroxidation. Resveratrol 92-103 mitogen-activated protein kinase 8 Homo sapiens 155-158 16322078-9 2006 In this respect, resveratrol acting through MAP kinase pathways and specifically on JNK could have a role other than acting as an antioxidant-quenching reactive oxygen intermediate. Resveratrol 17-28 mitogen-activated protein kinase 8 Homo sapiens 84-87 14661062-0 2004 Resveratrol inhibits phorbol myristate acetate-induced matrix metalloproteinase-9 expression by inhibiting JNK and PKC delta signal transduction. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 107-110 15217905-0 2005 Resveratrol induces FasL-related apoptosis through Cdc42 activation of ASK1/JNK-dependent signaling pathway in human leukemia HL-60 cells. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 76-79 15723279-5 2005 In the present study, we report that resveratrol, a phytoalexin present in grapes with known antioxidant and anti-inflammatory properties, attenuates high glucose-induced apoptotic changes, including c-Jun N-terminal kinase (JNK) activation and caspase-3 activation in human leukemia K562 cells. Resveratrol 37-48 mitogen-activated protein kinase 8 Homo sapiens 200-223 15723279-5 2005 In the present study, we report that resveratrol, a phytoalexin present in grapes with known antioxidant and anti-inflammatory properties, attenuates high glucose-induced apoptotic changes, including c-Jun N-terminal kinase (JNK) activation and caspase-3 activation in human leukemia K562 cells. Resveratrol 37-48 mitogen-activated protein kinase 8 Homo sapiens 225-228 15517885-4 2004 Resveratrol has been shown to suppress the activation of several transcription factors, including NF-kappaB, AP-1 and Egr-1; to inhibit protein kinases including IkappaBalpha kinase, JNK, MAPK, Akt, PKC, PKD and casein kinase II; and to down-regulate products of genes such as COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 183-186 14661062-7 2004 Resveratrol inhibited PMA-mediated activation of c-Jun N-terminal kinase (JNK) and protein kinase C (PKC)-delta activation. Resveratrol 0-11 mitogen-activated protein kinase 8 Homo sapiens 49-78 14661062-8 2004 Therefore, we conclude that the MMP-9 inhibition activity of resveratrol and its inhibition of JNK and PKC-delta may have a therapeutic potential, given that a novel means of controlling growth and invasiveness of tumors. Resveratrol 61-72 mitogen-activated protein kinase 8 Homo sapiens 95-98 11408617-4 2001 Pretreatment with resveratrol also inhibited the activation of extracellular signal-regulated protein kinase 2 (ERK2), c-jun N-terminal kinase 1 (JNK1), and p38. Resveratrol 18-29 mitogen-activated protein kinase 8 Homo sapiens 119-144 12510025-3 2003 trans-Resveratrol also reverses the sustained phosphorylation of JNK/SAPK, which specifically occurs after paclitaxel exposure.Overall, our observations demonstrate that (a) the toxic action of paclitaxel on neuronal-like cells is not only related to the effect of the drug on tubulin, but also to its capacity to activate several intracellular pathways leading to inactivation of Bcl-2, thus causing cells to die by apoptosis, (b) trans-resveratrol significantly reduces paclitaxel-induced apoptosis by modulating the cellular signaling pathways which commit the cell to apoptosis. Resveratrol 0-17 mitogen-activated protein kinase 8 Homo sapiens 65-73 12510025-3 2003 trans-Resveratrol also reverses the sustained phosphorylation of JNK/SAPK, which specifically occurs after paclitaxel exposure.Overall, our observations demonstrate that (a) the toxic action of paclitaxel on neuronal-like cells is not only related to the effect of the drug on tubulin, but also to its capacity to activate several intracellular pathways leading to inactivation of Bcl-2, thus causing cells to die by apoptosis, (b) trans-resveratrol significantly reduces paclitaxel-induced apoptosis by modulating the cellular signaling pathways which commit the cell to apoptosis. Resveratrol 432-449 mitogen-activated protein kinase 8 Homo sapiens 65-73 11408617-4 2001 Pretreatment with resveratrol also inhibited the activation of extracellular signal-regulated protein kinase 2 (ERK2), c-jun N-terminal kinase 1 (JNK1), and p38. Resveratrol 18-29 mitogen-activated protein kinase 8 Homo sapiens 146-150 10356984-1 1999 In porcine coronary arteries, short-term treatment with resveratrol (RSVL) substantially inhibited MAPK activity (IC50 = 37 microM); and immunoblot analyses revealed consistent reduction in the phosphorylation of ERK-1/-2, JNK-1 and p38, at active sites. Resveratrol 56-67 mitogen-activated protein kinase 8 Homo sapiens 223-228 10356984-1 1999 In porcine coronary arteries, short-term treatment with resveratrol (RSVL) substantially inhibited MAPK activity (IC50 = 37 microM); and immunoblot analyses revealed consistent reduction in the phosphorylation of ERK-1/-2, JNK-1 and p38, at active sites. Resveratrol 69-73 mitogen-activated protein kinase 8 Homo sapiens 223-228 33921192-6 2021 Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-beta1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. Resveratrol 37-48 mitogen-activated protein kinase 8 Homo sapiens 153-156