| Name | c Jun N terminal kinase (protein family or complex) |
|---|---|
| Synonyms | c Jun N terminal kinase; JNK; c Jun NH (2) terminal kinase; Jun N terminal kinase |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19777565 | Deng YT, Huang HC, Lin JK: Rotenone induces apoptosis in MCF-7 human breast cancer cell-mediated ROS through JNK and p38 signaling. Mol Carcinog. 2010 Feb;49(2):141-51. Moreover, the treatment of rotenone in MCF-7 cells caused the activation of c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPKs), and the inactivation of extracellular signal-regulated protein kinase 1/2 (ERK1/2). |
81(1,1,1,1) | Details |
| 17029596 | Hirata Y, Meguro T, Kiuchi K: Differential effect of nerve growth factor on dopaminergic neurotoxin-induced apoptosis. J Neurochem. 2006 Oct;99(2):416-25. There were distinct differences in intracellular mechanisms between rotenone- and -induced apoptosis such as the production of reactive species, the response to antioxidants, and the activation of the c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). |
81(1,1,1,1) | Details |
| 17356569 | Zhou F, Wu JY, Sun XL, Yao HH, Ding JH, Hu G: Iptakalim alleviates rotenone-induced degeneration of dopaminergic neurons through inhibiting microglia-mediated neuroinflammation. Neuropsychopharmacology. 2007 Dec;32(12):2570-80. Epub 2007 Mar 14. Furthermore, pretreatment with IPT prevented rotenone-induced mitochondrial membrane potential loss and p38/c-jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) activation in microglia, which might in turn regulate microglial activation and subsequent production of TNF-alpha and PGE (2). |
31(0,1,1,1) | Details |
| 17390063 | Choi KM, Kang CM, Cho ES, Kang SM, Lee SB, Um HD: Ionizing radiation-induced micronucleus formation is mediated by reactive species that are produced in a manner dependent on mitochondria, Nox1, and JNK. Oncol Rep. 2007 May;17(5):1183-8. IR also activated c-Jun N-terminal kinase (JNK), which was reversed by catalase, rotenone, or Nox1 RNA interference. |
31(0,1,1,1) | Details |
| 16787641 | Ito Y, Oh-Hashi K, Kiuchi K, Hirata Y: p44/42 MAP kinase and c-Jun N-terminal kinase contribute to the up-regulation of caspase-3 in -induced apoptosis in PC12 cells. Brain Res. 2006 Jul 12;1099(1):1-7. Epub 2006 Jun 19. Up-regulation of caspase-3 protein was evident in -treated PC12 cells and was moderate in cisplatin-, rotenone- and A23187-treated cells but was not observed in serum deprivation-, anisomycin-, camptothecin-, cycloheximide- or staurosporine-treated cells in which all treatments induced extensive DNA fragmentation. |
1(0,0,0,1) | Details |
| 15198987 | Jiang H, Ren Y, Zhao J, Feng J: Parkin protects human dopaminergic neuroblastoma cells against -induced apoptosis. Hum Mol Genet. 2004 Aug 15;13(16):1745-54. Epub 2004 Jun 15. Here, we show that overexpression of parkin protected human DA neuroblastoma cell line (SH-SY5Y) against apoptosis induced by DA or 6-OHDA, but not by H (2) O (2) or rotenone. Parkin significantly attenuated -induced activation of c-Jun N-terminal kinase (JNK) and caspase-3. |
1(0,0,0,1) | Details |
| 19012619 | Zhou F, Yao HH, Wu JY, Ding JH, Sun T, Hu G: Opening of microglial K (ATP) channels inhibits rotenone-induced neuroinflammation. J Cell Mol Med. 2008 Sep-Oct;12(5A):1559-70. Moreover, the underlying mechanisms involved the stabilization of mitochodrial membrane potential and inhibition of p38/c-Jun-N-terminal kinase (JNK) activation in microglia. |
1(0,0,0,1) | Details |
| 19807658 | Choi K, Kim J, Kim GW, Choi C: Oxidative stress-induced necrotic cell death via mitochondira-dependent burst of reactive species. Curr Neurovasc Res. 2009 Nov;6(4):213-22. peroxide induced non-apoptotic neuronal cell death in a c-Jun N-terminal kinase- and poly (ADP-ribosyl) polymerase-dependent manner. The inhibition of mitochondrial hyperpolarization by diphenylene iodonium or rotenone, potent inhibitors of mitochondrial respiratory chain complex I, resulted in reduced ROS production and subsequent neuronal cell death in vitro and in vivo. |
1(0,0,0,1) | Details |
| 17018646 | Ramachandiran S, Hansen JM, Jones DP, Richardson JR, Miller GW: Divergent mechanisms of paraquat, MPP+, and rotenone toxicity: oxidation of thioredoxin and caspase-3 activation. Toxicol Sci. 2007 Jan;95(1):163-71. Epub 2006 Oct 3. In this study, we show that paraquat specifically oxidized the cytosolic form of thioredoxin and activated Jun N-terminal kinase (JNK), followed by caspase-3 activation. |
1(0,0,0,1) | Details |
| 12730627 | Muscarella DE, O'Brien KA, Lemley AT, Bloom SE: Reversal of Bcl-2-mediated resistance of the EW36 human B-cell lymphoma cell line to arsenite- and pesticide-induced apoptosis by PK11195, a ligand of the mitochondrial benzodiazepine receptor. Toxicol Sci. 2003 Jul;74(1):66-73. Epub 2003 May 2. We found that, although EW36 cells are refractory to apoptosis induction by antimycin A, rotenone, pyridaben, alachlor, and carbonyl m-chlorophenylhydrazone (mClCCP), they are dramatically sensitized to induction of apoptosis by low concentrations of these same agents following pre-treatment with PK11195. Furthermore, using arsenite, we examined the role of the c-Jun N-terminal kinase (JNK) pathway and protein synthesis in apoptosis induction in EW36. |
1(0,0,0,1) | Details |
| 19196431 | Guglielmotto M, Aragno M, Autelli R, Giliberto L, Novo E, Colombatto S, Danni O, Parola M, Smith MA, Perry G, Tamagno E, Tabaton M: The up-regulation of BACE1 mediated by hypoxia and ischemic injury: role of oxidative stress and HIF1alpha. J Neurochem. 2009 Feb;108(4):1045-56. The involvement of reactive species released by mitochondria in the BACE1 up-regulation was confirmed by the complete protection exerted by complex I inhibitors such as rotenone and diphenyl-phenylen iodonium. Moreover, the oxidative stress-mediated up-regulation of BACE1 is mediated by c-jun N terminal kinase pathway as demonstrated by the protection exerted by the silencing of c-jun N-terminal kinase isoforms 1 and 2. |
1(0,0,0,1) | Details |