PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29334873-0 2018 Nobiletin prevents cadmium-induced neuronal apoptosis by inhibiting reactive oxygen species and modulating JNK/ERK1/2 and Akt/mTOR networks in rats. Cadmium 19-26 mitogen-activated protein kinase 8 Rattus norvegicus 107-110 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. Cadmium 128-130 mitogen-activated protein kinase 8 Rattus norvegicus 96-99 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. Cadmium 128-130 mitogen-activated protein kinase 8 Rattus norvegicus 321-324 28129433-0 2017 Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. Cadmium 22-24 mitogen-activated protein kinase 8 Rattus norvegicus 96-99 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Cadmium 32-39 mitogen-activated protein kinase 8 Rattus norvegicus 55-78 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Cadmium 32-39 mitogen-activated protein kinase 8 Rattus norvegicus 80-83 28129433-7 2017 Of importance, inhibiting NOX2 with apocynin or silencing NOX2 by RNA interference enhanced the inhibitory effects of celastrol on Cd-induced inactivation of PP5, activation of JNK/c-Jun, ROS, and apoptosis in the cells. Cadmium 131-133 mitogen-activated protein kinase 8 Rattus norvegicus 177-180 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Cadmium 32-39 mitogen-activated protein kinase 8 Rattus norvegicus 221-224 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Cadmium 41-43 mitogen-activated protein kinase 8 Rattus norvegicus 55-78 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Cadmium 41-43 mitogen-activated protein kinase 8 Rattus norvegicus 80-83 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Cadmium 41-43 mitogen-activated protein kinase 8 Rattus norvegicus 221-224 28129433-8 2017 Furthermore, we noticed that expression of wild-type PP5 or dominant negative c-Jun, or pretreatment with JNK inhibitor SP600125 reinforced celastrol"s suppression of Cd-induced NOX2 and its regulatory proteins, and consequential ROS in neuronal cells. Cadmium 167-169 mitogen-activated protein kinase 8 Rattus norvegicus 106-109 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. Cadmium 208-210 mitogen-activated protein kinase 8 Rattus norvegicus 80-83 28129433-9 2017 These findings indicate that celastrol ameliorates Cd-induced neuronal apoptosis via targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. Cadmium 51-53 mitogen-activated protein kinase 8 Rattus norvegicus 126-129 28129433-3 2017 Therefore, we hypothesized that celastrol could hinder Cd induction of ROS-dependent PP5-JNK signaling pathway from apoptosis in neuronal cells. Cadmium 55-57 mitogen-activated protein kinase 8 Rattus norvegicus 89-92 26164708-6 2015 Furthermore, L-theanine depresses cadmium-induced up regulation of phosphorylations of PI3K/Akt, MAPK ERK1/2, and JNK signaling. Cadmium 34-41 mitogen-activated protein kinase 8 Rattus norvegicus 114-117 26425111-4 2015 Cd also increased the phosphorylation of p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (JNK) in OBs. Cadmium 0-2 mitogen-activated protein kinase 8 Rattus norvegicus 138-161 26425111-4 2015 Cd also increased the phosphorylation of p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (JNK) in OBs. Cadmium 0-2 mitogen-activated protein kinase 8 Rattus norvegicus 163-166 24577723-0 2014 Cadmium induces PC12 cells apoptosis via an extracellular signal-regulated kinase and c-Jun N-terminal kinase-mediated mitochondrial apoptotic pathway. Cadmium 0-7 mitogen-activated protein kinase 8 Rattus norvegicus 86-109 25043952-5 2015 In addition, Cd induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 MAPK. Cadmium 13-15 mitogen-activated protein kinase 8 Rattus norvegicus 88-111 25043952-5 2015 In addition, Cd induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 MAPK. Cadmium 13-15 mitogen-activated protein kinase 8 Rattus norvegicus 113-116 25043952-6 2015 Inhibition of ERK and JNK, but not p38 MAPK, partially protected the cells from Cd-induced apoptosis. Cadmium 80-82 mitogen-activated protein kinase 8 Rattus norvegicus 22-25 25043952-8 2015 Taken together, these data suggest that the ERK- and JNK-mediated mitochondrial apoptotic pathways play important roles in Cd-induced neuronal apoptosis. Cadmium 123-125 mitogen-activated protein kinase 8 Rattus norvegicus 53-56 24577723-2 2014 The result showed that Cd significantly decreased cell viability and the Bcl-2 / Bax ratio and increased the percentage of apoptotic cells, release of cytochrome c, caspase-3, and poly(ADP-ribose) polymerase cleavage, and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G. In addition, exposure to Cd-induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. Cadmium 23-25 mitogen-activated protein kinase 8 Rattus norvegicus 399-422 24577723-2 2014 The result showed that Cd significantly decreased cell viability and the Bcl-2 / Bax ratio and increased the percentage of apoptotic cells, release of cytochrome c, caspase-3, and poly(ADP-ribose) polymerase cleavage, and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G. In addition, exposure to Cd-induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. Cadmium 23-25 mitogen-activated protein kinase 8 Rattus norvegicus 424-427 24577723-3 2014 Inhibition of ERK and JNK, but not p38 MAPK, partially protected the cells from Cd-induced apoptosis. Cadmium 80-82 mitogen-activated protein kinase 8 Rattus norvegicus 22-25 24577723-5 2014 Taken together, these data suggest that the ERK- and JNK-mediated mitochondrial apoptotic pathway played an important role in Cd-induced PC12 cells apoptosis. Cadmium 126-128 mitogen-activated protein kinase 8 Rattus norvegicus 53-56 16568437-0 2006 Acquisition of apoptotic resistance in cadmium-induced malignant transformation: specific perturbation of JNK signal transduction pathway and associated metallothionein overexpression. Cadmium 39-46 mitogen-activated protein kinase 8 Rattus norvegicus 106-109 16516943-8 2006 Ro318220, a strong activator of JNK, reverted cadmium-sensitive phenotype in adapted cells. Cadmium 46-53 mitogen-activated protein kinase 8 Rattus norvegicus 32-35 16516943-9 2006 Taken together, our results suggest that during cadmium adaptation, cells develop tolerance to cell death, generally due to perturbation of the JNK signaling pathway and the nonresponsiveness of JNK phosphorylation is critical for the Cd-tolerance in these cells. Cadmium 48-55 mitogen-activated protein kinase 8 Rattus norvegicus 144-147 16516943-9 2006 Taken together, our results suggest that during cadmium adaptation, cells develop tolerance to cell death, generally due to perturbation of the JNK signaling pathway and the nonresponsiveness of JNK phosphorylation is critical for the Cd-tolerance in these cells. Cadmium 48-55 mitogen-activated protein kinase 8 Rattus norvegicus 195-198 16516943-7 2006 Treatment of cells with high levels of cadmium resulted in decreased phosphorylation of c-Jun N-terminal kinase (JNK1/2) in adapted cells than in sensitive cells and this cadmium-induced JNK activity was blocked by JNK inhibitor II, SP600125. Cadmium 39-46 mitogen-activated protein kinase 8 Rattus norvegicus 113-116 16516943-7 2006 Treatment of cells with high levels of cadmium resulted in decreased phosphorylation of c-Jun N-terminal kinase (JNK1/2) in adapted cells than in sensitive cells and this cadmium-induced JNK activity was blocked by JNK inhibitor II, SP600125. Cadmium 39-46 mitogen-activated protein kinase 8 Rattus norvegicus 187-190 16516943-7 2006 Treatment of cells with high levels of cadmium resulted in decreased phosphorylation of c-Jun N-terminal kinase (JNK1/2) in adapted cells than in sensitive cells and this cadmium-induced JNK activity was blocked by JNK inhibitor II, SP600125. Cadmium 171-178 mitogen-activated protein kinase 8 Rattus norvegicus 113-116 16516943-7 2006 Treatment of cells with high levels of cadmium resulted in decreased phosphorylation of c-Jun N-terminal kinase (JNK1/2) in adapted cells than in sensitive cells and this cadmium-induced JNK activity was blocked by JNK inhibitor II, SP600125. Cadmium 171-178 mitogen-activated protein kinase 8 Rattus norvegicus 187-190 16568437-6 2006 JNK kinase activity was also suppressed in CCE-LE cells exposed to cadmium. Cadmium 67-74 mitogen-activated protein kinase 8 Rattus norvegicus 0-3 16568437-11 2006 These results indicate cadmium-transformed cells acquired apoptotic resistance, which may be linked to the specific suppression of the JNK pathway and is associated with MT overexpression, which, in turn, may impact this signal transduction pathway. Cadmium 23-30 mitogen-activated protein kinase 8 Rattus norvegicus 135-138 15252869-0 2004 Characterization of Cd-induced molecular events prior to cellular damage in primary rat hepatocytes in culture: activation of the stress activated signal protein JNK and transcription factor AP-1. Cadmium 20-22 mitogen-activated protein kinase 8 Rattus norvegicus 162-165 15740985-11 2005 V-PYRRO/NO pretreatment also markedly reduced apoptotic cell death induced by cadmium (5 microM), apparently by blocking cadmium-induced activation of the c-Jun N-terminal kinase (JNK) pathway. Cadmium 78-85 mitogen-activated protein kinase 8 Rattus norvegicus 155-178 15740985-11 2005 V-PYRRO/NO pretreatment also markedly reduced apoptotic cell death induced by cadmium (5 microM), apparently by blocking cadmium-induced activation of the c-Jun N-terminal kinase (JNK) pathway. Cadmium 78-85 mitogen-activated protein kinase 8 Rattus norvegicus 180-183 15740985-11 2005 V-PYRRO/NO pretreatment also markedly reduced apoptotic cell death induced by cadmium (5 microM), apparently by blocking cadmium-induced activation of the c-Jun N-terminal kinase (JNK) pathway. Cadmium 121-128 mitogen-activated protein kinase 8 Rattus norvegicus 155-178 15740985-11 2005 V-PYRRO/NO pretreatment also markedly reduced apoptotic cell death induced by cadmium (5 microM), apparently by blocking cadmium-induced activation of the c-Jun N-terminal kinase (JNK) pathway. Cadmium 121-128 mitogen-activated protein kinase 8 Rattus norvegicus 180-183 15252869-1 2004 The effect of Cadmium (Cd) on the expression of c-Jun N-terminal kinase (JNK), c-jun, and activator protein-1 (AP-1) has been investigated. Cadmium 14-21 mitogen-activated protein kinase 8 Rattus norvegicus 48-71 15252869-1 2004 The effect of Cadmium (Cd) on the expression of c-Jun N-terminal kinase (JNK), c-jun, and activator protein-1 (AP-1) has been investigated. Cadmium 14-21 mitogen-activated protein kinase 8 Rattus norvegicus 73-76 15252869-1 2004 The effect of Cadmium (Cd) on the expression of c-Jun N-terminal kinase (JNK), c-jun, and activator protein-1 (AP-1) has been investigated. Cadmium 23-25 mitogen-activated protein kinase 8 Rattus norvegicus 48-71 15252869-1 2004 The effect of Cadmium (Cd) on the expression of c-Jun N-terminal kinase (JNK), c-jun, and activator protein-1 (AP-1) has been investigated. Cadmium 23-25 mitogen-activated protein kinase 8 Rattus norvegicus 73-76 15252869-4 2004 We propose that Cd, through the generation of reactive oxygen species (ROS) and prior to significant cellular damage, activates the stress activated signal protein JNK, regulates c-jun expression, and promotes the binding of a redox sensitive transcription factor AP-1. Cadmium 16-18 mitogen-activated protein kinase 8 Rattus norvegicus 164-167 15252869-6 2004 Blocking the Cd induction of JNK activity, c-jun mRNA level, and AP-1 binding activity using the antioxidants N-acetyl cysteine (10 mM) or carnosol (0.5 microg/mL) suggests a role for ROS. Cadmium 13-15 mitogen-activated protein kinase 8 Rattus norvegicus 29-32 11312036-2 2001 Previous studies revealed that sulfur amino acid deprivation (SAAD) activated MAP kinases and potentiated cadmium-induced cytotoxicity by activation of ERK1/2 in conjunction with p38 kinase or JNK. Cadmium 106-113 mitogen-activated protein kinase 8 Rattus norvegicus 193-196 15252869-7 2004 Blocking JNK activity and c-jun mRNA by SP600125 (20 microM), a JNK inhibitor, supports the role of JNK in transmission of signals induced by Cd. Cadmium 142-144 mitogen-activated protein kinase 8 Rattus norvegicus 9-12 15252869-7 2004 Blocking JNK activity and c-jun mRNA by SP600125 (20 microM), a JNK inhibitor, supports the role of JNK in transmission of signals induced by Cd. Cadmium 142-144 mitogen-activated protein kinase 8 Rattus norvegicus 64-67 15252869-7 2004 Blocking JNK activity and c-jun mRNA by SP600125 (20 microM), a JNK inhibitor, supports the role of JNK in transmission of signals induced by Cd. Cadmium 142-144 mitogen-activated protein kinase 8 Rattus norvegicus 64-67 34767868-8 2022 Cd-induced activation of MAPK and PI3K/Akt signaling pathways were inhibited by gamma-GC treatment, while sustained phosphorylation of JNK, p38, or Akt reversed anti-apoptotic effects of gamma-GC. Cadmium 0-2 mitogen-activated protein kinase 8 Rattus norvegicus 135-138 34185081-4 2021 Here, we demonstrate that activation of caspase-8 and the JNK pathway are mechanisms underlying Cd-induced Fas-mediated activation of the mitochondrial apoptotic pathway in rat cerebral cortical neurons. Cadmium 96-98 mitogen-activated protein kinase 8 Rattus norvegicus 58-61 34185081-5 2021 In vitro, Cd induced apoptosis in primary cortical neurons by activating caspase-8, JNK, and the mitochondrial apoptotic pathway. Cadmium 10-12 mitogen-activated protein kinase 8 Rattus norvegicus 84-87 34185081-6 2021 Fas knockdown enhanced cell viability in the presence of Cd, and inhibited apoptosis by blocking Cd-activated Fas, caspase-8, and JNK. Cadmium 57-59 mitogen-activated protein kinase 8 Rattus norvegicus 130-133 30715683-13 2019 These results indicate that administration of GSH was effective in attenuating Cd-induced oxidative stress via decreasing Cd uptake, restoring the activities of oxidative enzymes, activating NF-kappaB, inhibiting the JNK signaling pathway, and preventing excessive ROS generation and HSC activation. Cadmium 79-81 mitogen-activated protein kinase 8 Rattus norvegicus 217-220 34021889-0 2021 Cadmium Impairs Autophagy Leading to Apoptosis by Ca2+-Dependent Activation of JNK Signaling Pathway in Neuronal Cells. Cadmium 0-7 mitogen-activated protein kinase 8 Rattus norvegicus 79-82 31348969-0 2019 Cadmium exposure induces pancreatic beta-cell death via a Ca2+-triggered JNK/CHOP-related apoptotic signaling pathway. Cadmium 0-7 mitogen-activated protein kinase 8 Rattus norvegicus 73-76 31348969-7 2019 Cd exposure induced apoptotic events, including the increased populations of apoptotic cells and sub-G1 hypodiploid cells, and caspase-3/-7/-9 and poly (ADP-ribose) polymerase (PARP) activation, which largely depended on the activation of c-Jun N-terminal kinase (JNK) and C/EBP homologous protein (CHOP). Cadmium 0-2 mitogen-activated protein kinase 8 Rattus norvegicus 239-262 31348969-12 2019 Taken together, these findings demonstrated that Cd exposure exerts beta-cell death via a [Ca2+]i-dependent JNK activation-activated downstream CHOP-related apoptotic signaling pathway. Cadmium 49-51 mitogen-activated protein kinase 8 Rattus norvegicus 108-111 31348969-7 2019 Cd exposure induced apoptotic events, including the increased populations of apoptotic cells and sub-G1 hypodiploid cells, and caspase-3/-7/-9 and poly (ADP-ribose) polymerase (PARP) activation, which largely depended on the activation of c-Jun N-terminal kinase (JNK) and C/EBP homologous protein (CHOP). Cadmium 0-2 mitogen-activated protein kinase 8 Rattus norvegicus 264-267 31348969-8 2019 Transfection with siRNAs for JNK and CHOP or pretreatment with specific pharmacological inhibitor of JNK (SP600125) in beta-cells effectively prevented the Cd-induced insulin secretion dysfunction and apoptosis. Cadmium 156-158 mitogen-activated protein kinase 8 Rattus norvegicus 29-32 31348969-8 2019 Transfection with siRNAs for JNK and CHOP or pretreatment with specific pharmacological inhibitor of JNK (SP600125) in beta-cells effectively prevented the Cd-induced insulin secretion dysfunction and apoptosis. Cadmium 156-158 mitogen-activated protein kinase 8 Rattus norvegicus 101-104 31348969-9 2019 JNK-specific siRNA dramatically suppressed Cd-induced JNK phosphorylation and CHOP protein expression, but JNK phosphorylation could not be inhibited by CHOP-specific siRNA. Cadmium 43-45 mitogen-activated protein kinase 8 Rattus norvegicus 0-3 31348969-9 2019 JNK-specific siRNA dramatically suppressed Cd-induced JNK phosphorylation and CHOP protein expression, but JNK phosphorylation could not be inhibited by CHOP-specific siRNA. Cadmium 43-45 mitogen-activated protein kinase 8 Rattus norvegicus 54-57 31348969-9 2019 JNK-specific siRNA dramatically suppressed Cd-induced JNK phosphorylation and CHOP protein expression, but JNK phosphorylation could not be inhibited by CHOP-specific siRNA. Cadmium 43-45 mitogen-activated protein kinase 8 Rattus norvegicus 54-57 31348969-11 2019 Buffering the Ca2+ response with BAPTA/AM effectively abrogated the Cd-induced [Ca2+]i elevation, insulin secretion dysfunction, apoptosis, and protein expression of JNK phosphorylation and CHOP activation. Cadmium 68-70 mitogen-activated protein kinase 8 Rattus norvegicus 166-169