PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25806604-0 2015 Activation of JNK pathway in spinal astrocytes contributes to acute ultra-low-dose morphine thermal hyperalgesia. Morphine 83-91 mitogen-activated protein kinase 8 Homo sapiens 14-17 26056051-1 2015 G protein-coupled receptor desensitization is typically mediated by receptor phosphorylation by G protein-coupled receptor kinase (GRK) and subsequent arrestin binding; morphine, however, was previously found to activate a c-Jun N-terminal kinase (JNK)-dependent, GRK/arrestin-independent pathway to produce mu opioid receptor (MOR) inactivation in spinally-mediated, acute anti-nociceptive responses [Melief et al.] Morphine 169-177 mitogen-activated protein kinase 8 Homo sapiens 248-251 25806604-7 2015 Morphine elevated spinal JNK1, JNK2, and c-Jun phosphorylation. Morphine 0-8 mitogen-activated protein kinase 8 Homo sapiens 25-29 25806604-11 2015 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine 44-52 mitogen-activated protein kinase 8 Homo sapiens 125-128 25806604-11 2015 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine 44-52 mitogen-activated protein kinase 8 Homo sapiens 125-128 25806604-11 2015 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine 233-241 mitogen-activated protein kinase 8 Homo sapiens 70-73 25806604-11 2015 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine 233-241 mitogen-activated protein kinase 8 Homo sapiens 125-128 25806604-11 2015 Pretreatment with a PKC inhibitor prevented morphine hyperalgesia and JNK and c-Jun overphosphorylation, indicating PKC is a JNK upstream modulator and illustrating the presence of a pathway involving PKC, NMDA, and JNK activated by morphine. Morphine 233-241 mitogen-activated protein kinase 8 Homo sapiens 125-128 25806604-14 2015 These results illustrate the selective activation of an astrocyte JNK pathway after the stimulation of neuronal MOR, which contributes to ultra-low-dose morphine hyperalgesia. Morphine 153-161 mitogen-activated protein kinase 8 Homo sapiens 66-69 26065412-0 2015 Tolerance to the antinociceptive effects of chronic morphine requires c-Jun N-terminal kinase. Morphine 52-60 mitogen-activated protein kinase 8 Homo sapiens 70-93 26065412-4 2015 Recent studies have found that tolerance to morphine is mediated by the c-Jun N-terminal Kinase (JNK) signaling pathway. Morphine 44-52 mitogen-activated protein kinase 8 Homo sapiens 72-95 26065412-4 2015 Recent studies have found that tolerance to morphine is mediated by the c-Jun N-terminal Kinase (JNK) signaling pathway. Morphine 44-52 mitogen-activated protein kinase 8 Homo sapiens 97-100 26065412-5 2015 The goal of the present study was to test the hypotheses that: 1) JNK inhibition will be antinociceptive on its own; 2) JNK inhibition will augment morphine antinociception and; 3) JNK mediates chronic tolerance for the antinociceptive effects of morphine using acute (hotplate and tail-flick), inflammatory (10 mul of formalin 2.5%) and chemotherapy (cisplatin 5 mg/kg ip once weekly)-induced neuropathic pain assays. Morphine 148-156 mitogen-activated protein kinase 8 Homo sapiens 120-123 26065412-5 2015 The goal of the present study was to test the hypotheses that: 1) JNK inhibition will be antinociceptive on its own; 2) JNK inhibition will augment morphine antinociception and; 3) JNK mediates chronic tolerance for the antinociceptive effects of morphine using acute (hotplate and tail-flick), inflammatory (10 mul of formalin 2.5%) and chemotherapy (cisplatin 5 mg/kg ip once weekly)-induced neuropathic pain assays. Morphine 148-156 mitogen-activated protein kinase 8 Homo sapiens 120-123 26065412-6 2015 RESULTS: We found that JNK inhibition by SP600125 (3 mg/kg) produces a greater antinociceptive effect than morphine (6 mg/kg) alone in the formalin test. Morphine 107-115 mitogen-activated protein kinase 8 Homo sapiens 23-26 26065412-13 2015 CONCLUSIONS: These results demonstrate that JNK signaling plays a crucial role in mediating antinociception as well as chronic tolerance to the antinociceptive effects of morphine in acute, inflammatory, and neuropathic pain states. Morphine 171-179 mitogen-activated protein kinase 8 Homo sapiens 44-47 26065412-14 2015 Thus, inhibition of JNK signaling pathway, via SP600125, represents an efficacious pharmacological approach to delay tolerance to the antinociceptive effects of chronic morphine in diverse pain models. Morphine 169-177 mitogen-activated protein kinase 8 Homo sapiens 20-23 23555556-10 2013 In addition, AKT, p38, and JNK pathways were involved in morphine-induced down regulation of SDCM in human podocytes. Morphine 57-65 mitogen-activated protein kinase 8 Homo sapiens 27-30 23932892-3 2013 Exposure of differentiated cells to morphine dose-dependently induced apoptosis in these cells through c-Jun N-terminal kinase (JNK)/caspase pathway. Morphine 36-44 mitogen-activated protein kinase 8 Homo sapiens 103-126 23932892-3 2013 Exposure of differentiated cells to morphine dose-dependently induced apoptosis in these cells through c-Jun N-terminal kinase (JNK)/caspase pathway. Morphine 36-44 mitogen-activated protein kinase 8 Homo sapiens 128-131 23485395-3 2013 Several in vivo and in vitro studies have shown that the c-Jun NH2-terminal kinase (JNK) pathway is closely associated with neuropathic hyperalgesia, which closely resembles the neuroplastic changes observed with morphine antinociceptive tolerance. Morphine 213-221 mitogen-activated protein kinase 8 Homo sapiens 57-82 23485395-3 2013 Several in vivo and in vitro studies have shown that the c-Jun NH2-terminal kinase (JNK) pathway is closely associated with neuropathic hyperalgesia, which closely resembles the neuroplastic changes observed with morphine antinociceptive tolerance. Morphine 213-221 mitogen-activated protein kinase 8 Homo sapiens 84-87 19292871-0 2009 Chronic high-dose morphine treatment promotes SH-SY5Y cell apoptosis via c-Jun N-terminal kinase-mediated activation of mitochondria-dependent pathway. Morphine 18-26 mitogen-activated protein kinase 8 Homo sapiens 73-96 21483469-7 2011 Extensive studies of mitogen activated protein kinase (MAPK) signaling pathways revealed the involvement of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase-1/2 (ERK1/2) pathways in enhanced toxicity of Tat and morphine. Morphine 234-242 mitogen-activated protein kinase 8 Homo sapiens 108-131 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. Morphine 43-51 mitogen-activated protein kinase 8 Homo sapiens 96-99 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. Morphine 43-51 mitogen-activated protein kinase 8 Homo sapiens 219-222 19292871-3 2009 Here we show that c-Jun N-terminal kinase (JNK) plays a pivotal role in high-dose morphine-induced apoptosis of SH-SY5Y cells in a mitochondria-dependent manner. Morphine 82-90 mitogen-activated protein kinase 8 Homo sapiens 18-41 19292871-3 2009 Here we show that c-Jun N-terminal kinase (JNK) plays a pivotal role in high-dose morphine-induced apoptosis of SH-SY5Y cells in a mitochondria-dependent manner. Morphine 82-90 mitogen-activated protein kinase 8 Homo sapiens 43-46 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. Morphine 21-29 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. Morphine 206-214 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. Morphine 206-214 mitogen-activated protein kinase 8 Homo sapiens 191-194 19292871-7 2009 All of these effects of morphine could be suppressed by the JNK inhibitor SP600125 and N-acetylcysteine. Morphine 24-32 mitogen-activated protein kinase 8 Homo sapiens 60-63 19292871-8 2009 The key role of the JNK pathway in morphine-induced apoptosis was further confirmed by the observation that decreased levels of JNK in cells transfected with specific small interfering RNA resulted in resistance to the proapoptotic effect of morphine. Morphine 35-43 mitogen-activated protein kinase 8 Homo sapiens 20-23 19292871-8 2009 The key role of the JNK pathway in morphine-induced apoptosis was further confirmed by the observation that decreased levels of JNK in cells transfected with specific small interfering RNA resulted in resistance to the proapoptotic effect of morphine. Morphine 35-43 mitogen-activated protein kinase 8 Homo sapiens 128-131 19292871-8 2009 The key role of the JNK pathway in morphine-induced apoptosis was further confirmed by the observation that decreased levels of JNK in cells transfected with specific small interfering RNA resulted in resistance to the proapoptotic effect of morphine. Morphine 242-250 mitogen-activated protein kinase 8 Homo sapiens 20-23 19292871-8 2009 The key role of the JNK pathway in morphine-induced apoptosis was further confirmed by the observation that decreased levels of JNK in cells transfected with specific small interfering RNA resulted in resistance to the proapoptotic effect of morphine. Morphine 242-250 mitogen-activated protein kinase 8 Homo sapiens 128-131 18509045-7 2008 Intrathecal administration of the selective p38, ERK, or JNK inhibitors not only reduced morphine tolerance and associated thermal hyperalgesia but also suppressed the morphine-induced increase of TRPV1-IR in DRG neurons, spinal cord, and sciatic nerve and of mRNA levels in spinal cord and sciatic nerve. Morphine 168-176 mitogen-activated protein kinase 8 Homo sapiens 57-60 18509045-6 2008 Chronic morphine exposure induced increases in phosphorylation of mitogen-activated protein kinases (MAPKs), including p38 MAPK-IR, extracellular signal-regulated protein kinase (ERK)-IR, and c-Jun N-terminal kinase (JNK)-IR, in L4 DRG neurons. Morphine 8-16 mitogen-activated protein kinase 8 Homo sapiens 217-220 18509045-7 2008 Intrathecal administration of the selective p38, ERK, or JNK inhibitors not only reduced morphine tolerance and associated thermal hyperalgesia but also suppressed the morphine-induced increase of TRPV1-IR in DRG neurons, spinal cord, and sciatic nerve and of mRNA levels in spinal cord and sciatic nerve. Morphine 89-97 mitogen-activated protein kinase 8 Homo sapiens 57-60