| Name | c jun |
|---|---|
| Synonyms | AP1; Activator protein 1; JUN; Proto oncogene c jun; Protooncogene c jun; Transcription factor AP 1; V jun avian sarcoma virus 17 oncogene homolog; c Jun… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17324951 | Klintworth H, Newhouse K, Li T, Choi WS, Faigle R, Xia Z: Activation of c-Jun N-terminal protein kinase is a common mechanism underlying paraquat- and rotenone-induced dopaminergic cell apoptosis. Toxicol Sci. 2007 May;97(1):149-62. Epub 2007 Feb 25. |
162(2,2,2,2) | Details |
| 14976342 | Newhouse K, Hsuan SL, Chang SH, Cai B, Wang Y, Xia Z: Rotenone-induced apoptosis is mediated by p38 and JNK MAP kinases in human dopaminergic SH-SY5Y cells. Toxicol Sci. 2004 May;79(1):137-46. Epub 2004 Feb 19. Furthermore, rotenone treatment induces phosphorylation of c-Jun, the c-Jun N-terminal protein kinase (JNK), and the p38 mitogen activated protein (MAP) kinase, indicative of activation of the p38 and JNK pathways. |
81(1,1,1,1) | Details |
| 18242171 | Chen S, Zhang X, Yang D, Du Y, Li L, Li X, Ming M, Le W: D2/D3 receptor agonist ropinirole protects dopaminergic cell line against rotenone-induced apoptosis through inhibition of caspase- and JNK-dependent pathways. FEBS Lett. 2008 Mar 5;582(5):603-10. Epub 2008 Jan 31. We found that ropinirole can block the rotenone-induced phosphorylation of JNK, P38 and p-c-Jun, but promote the phosphorylation of ERK1/2. |
81(1,1,1,1) | Details |
| 18832435 | Hu LF, Lu M, Wu ZY, Wong PT, Bian JS: inhibits rotenone-induced apoptosis via preservation of mitochondrial function. Mol Pharmacol. 2009 Jan;75(1):27-34. Epub 2008 Oct 2. NaHS also prevented rotenone-induced p38- and c-Jun NH (2)-terminal kinase (JNK)-mitogen-activated protein kinase (MAPK) phosphorylation and rotenone-mediated changes in Bcl-2/Bax levels, mitochondrial membrane potential (DeltaPsi (m)) dissipation, cytochrome c release, caspase-9/3 activation and poly (ADP- polymerase cleavage. |
31(0,1,1,1) | Details |
| 10780954 | Lin Z, Weinberg JM, Malhotra R, Merritt SE, Holzman LB, Brosius FC 3rd: GLUT-1 reduces hypoxia-induced apoptosis and JNK pathway activation. . Am J Physiol Endocrinol Metab. 2000 May;278(5):E958-66. In addition, hypoxia and rotenone stimulated c-Jun-NH (2)-terminal kinase (JNK) activity > 10-fold in control cell lines, and this activation was markedly reduced in GLUT-1-overexpressing cell lines. |
31(0,1,1,1) | Details |
| 19874289 | Avila-Gomez IC, Velez-Pardo C, Jimenez-Del-Rio M: Effects of insulin-like growth factor-1 on rotenone-induced apoptosis in human lymphocyte cells. Basic Clin Pharmacol Toxicol. 2010 Jan;106(1):53-61. Epub 2009 Oct 28. The present work shows that rotenone, a mitochondrial complex I inhibitor, induced time- and concentration-dependent apoptosis in lymphocytes which was mediated by anion radicals (O (2)*(-))/ peroxide, depolarization of mitochondria, caspase-3 activation, concomitantly with the nuclear translocation of transcription factors such as NF-kappaB, p53, c-Jun and nuclei fragmentation. |
31(0,1,1,1) | Details |
| 16572112 | Lin CL, Wang FS, Kuo YR, Huang YT, Huang HC, Sun YC, Kuo YH: Ras modulation of activates ERK-dependent fibronectin expression in diabetes-induced renal injuries. Kidney Int. 2006 May;69(9):1593-600. Transforming growth factor (TGF)-beta1, fibronectin expression, Ras, ERK, p38, and c-Jun activation of glomerular mesangial cells or urinary albumin secretion were assessed. Pretreatment with diphenyliodonium, not allopurinol or rotenone, reduced high- and AGE augmentation of synthesis and fibronection expression. |
3(0,0,0,3) | Details |
| 15557194 | Woo CH, Lim JH, Kim JH: Lipopolysaccharide induces matrix metalloproteinase-9 expression via a mitochondrial reactive species-p38 kinase-activator protein-1 pathway in Raw 264.7 cells. J Immunol. 2004 Dec 1;173(11):6973-80. LPS-induced MMP-9 expression and p38 kinase phosphorylation were also inhibited by rotenone, a specific inhibitor of mitochondrial complex I, supporting the role of mitochondrial ROS in LPS signaling to MMP-9. |
2(0,0,0,2) | Details |
| 17881465 | Ding G, Zhang A, Huang S, Pan X, Zhen G, Chen R, Yang T: ANG II induces c-Jun NH2-terminal kinase activation and proliferation of human mesangial cells via redox-sensitive transactivation of the EGFR. Am J Physiol Renal Physiol. 2007 Dec;293(6):F1889-97. Epub 2007 Sep 19. In contrast, inhibitors of other oxidant-producing enzymes, including the mitochondrial complex I inhibitor rotenone, the xanthine oxidase inhibitor allopurinol, the cyclooxygenase inhibitor indomethacin, the lipoxygenase inhibitor nordihydroguiaretic acid, the cytochrome P-450 oxygenase inhibitor ketoconazole, and the synthase inhibitor N (G)-nitro- methyl ester, were without effect. |
2(0,0,0,2) | Details |
| 12208513 | Wu HM, Chi KH, Lin WW: Proteasome inhibitors stimulate activator protein-1 pathway via reactive species production. FEBS Lett. 2002 Aug 28;526(1-3):101-5. The stimulating effects on IL-8 promoter and AP-1 were reduced by diphenyleneiodonium, rotenone and antimycin A. |
2(0,0,0,2) | Details |
| 18218673 | Jin S, Ray RM, Johnson LR: TNF-alpha/cycloheximide-induced apoptosis in intestinal epithelial cells requires Rac1-regulated reactive species. Am J Physiol Gastrointest Liver Physiol. 2008 Apr;294(4):G928-37. Epub 2008 Jan 24. 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 species (ROS) in apoptosis is unclear. The antioxidant, (NAC), or rotenone (Rot), the mitochondrial electron transport chain inhibitor, attenuated mitochondrial ROS production and apoptosis. |
1(0,0,0,1) | Details |
| 15485993 | Pignatelli M, Sanchez-Rodriguez J, Santos A, Perez-Castillo A: 15-deoxy-Delta-12,14- induces programmed cell death of breast cancer cells by a pleiotropic mechanism. Carcinogenesis. 2005 Jan;26(1):81-92. Epub 2004 Oct 14. In addition to PPARgamma activation other proteins, such as NF-kappaB and AP1, have been shown to be targets of 15dPG-J2. In contrast, the addition of radical scavengers or rotenone, which prevent 15dPG-J2-induced ROS production, block the loss of cell viability induced by this prostaglandin. |
1(0,0,0,1) | Details |
| 10571731 | Corsini E, Asti L, Viviani B, Marinovich M, Galli CL: arsenate induces overproduction of interleukin-1alpha in murine keratinocytes: role of mitochondria. J Invest Dermatol. 1999 Nov;113(5):760-5. This effect could be prevented by rotenone pretreatment, which suggests the possible involvement of mitochondria-derived reactive species. Arsenic induced a concentration- and time-dependent increase in cellular oxidative activity, which was followed by activation of redox-sensitive transcription factors such as nuclear factor-kappaB and activator protein-1, that are essential for interleukin-1alpha synthesis. |
1(0,0,0,1) | Details |
| 11382920 | Hoffmann A, Gloe T, Pohl U: Hypoxia-induced upregulation of eNOS gene expression is redox-sensitive: a comparison between hypoxia and inhibitors of cell metabolism. J Cell Physiol. 2001 Jul;188(1):33-44. In order to study a potential role of the redox regulated transcription factor complex AP-1 in hypoxia-induced eNOS mRNA transcription, c-jun expression was determined and decoy experiments were performed. c-jun expression paralleled changes of eNOS mRNA expression and MTT-reduction. Therefore, cultured porcine aortic endothelial cells (PAEC) were exposed to hypoxia (1-10% O (2)) or inhibitors of cellular energy metabolism including rotenone, 2, 4 dinitrophenol (DNP) and 2-deoxyglucose for 6 to 24 h. |
1(0,0,0,1) | Details |
| 18481258 | Wu F, Tyml K, Wilson JX: iNOS expression requires oxidase-dependent redox signaling in microvascular endothelial cells. J Cell Physiol. 2008 Oct;217(1):207-14. Unstimulated endothelial cells produced reactive species (ROS) sensitive to inhibition of oxidase (apocynin and DPI), mitochondrial respiration (rotenone) and NOS (L-NAME). LPS + IFNgamma-stimulated oxidase activity produces ROS that activate the JNK-AP1 and Jak2-IRF1 signaling pathways required for iNOS induction. |
1(0,0,0,1) | Details |
| 15479985 | Ichikawa H, Kokura S, Aw TY: Role of endothelial mitochondria in oxidant production and modulation of neutrophil adherence. J Vasc Res. 2004 Sep-Oct;41(5):432-44. Epub 2004 Oct 12. Blockade of electron transport in antimycin A and A/R exposed cells with rotenone, amytal or thenoyltrifluoroacetate, but not myxothiazol, prevented neutrophil adhesion, confirming a role for mitochondrial ROS. Actinomycin D and cycloheximide or competing ds-oligonucleotides containing cognate DNA sequences of the nuclear factor kappaB or activator protein-1 attenuated phase 2 adhesion, implicating a role for de novo protein synthesis. |
1(0,0,0,1) | Details |