| Name | MAPK (protein family or complex) |
|---|---|
| Synonyms | MAPK; mitogen activated protein kinase; mitogen activated protein kinases |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16651638 | Watanabe N, Zmijewski JW, Takabe W, Umezu-Goto M, Le Goffe C, Sekine A, Landar A, Watanabe A, Aoki J, Arai H, Kodama T, Murphy MP, Kalyanaraman R, Darley-Usmar VM, Noguchi N: Activation of mitogen-activated protein kinases by lysophosphatidylcholine-induced mitochondrial reactive species generation in endothelial cells. Am J Pathol. 2006 May;168(5):1737-48. ERK activation was attenuated by inhibitors of the electron transport chain proton pumps (rotenone and antimycin A) and an uncoupler (carbonyl p-trifluoromethoxyphenylhydrazone), suggesting that mitochondrial inner membrane potential plays a key role in the signaling pathway. |
3(0,0,0,3) | Details |
| 19610261 | Lee YA, Shin MH: Mitochondrial respiration is required for activation of ERK1/2 and caspase-3 in human eosinophils stimulated with peroxide. J Investig Allergol Clin Immunol. 2009;19(3):188-94. In this study, we investigated the role of mitochondrial ROS in the activation of extracellular signal-regulated kinases (ERK) 1 and 2-mitogen-activated protein kinase (MAPK) and caspase-3 in human eosinophils stimulated with H2O2. Eosinophils were pretreated with rotenone, an inhibitor of the mitochondrial electron transport chain, before H2O2 was added. |
2(0,0,0,2) | Details |
| 19737348 | Martin R, Hernandez M, Ibeas E, Fuentes L, Salicio V, Arnes M, Nieto ML: Secreted phospholipase A2-IIA modulates key regulators of proliferation on astrocytoma cells. J Neurochem. 2009 Nov;111(4):988-99. Epub 2009 Sep 8. We have previously demonstrated that exogenous sPLA (2)-IIA, by engagement to a membrane structure, induces proliferation and activation of mitogen-activated protein kinases cascade in human astrocytoma cells. We found that sPLA (2)-IIA promoted reactive species (ROS) accumulation, which was abrogated in the presence of allopurinol and DPI, but not by rotenone, discarding mitochondria as a ROS source. |
1(0,0,0,1) | 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. These results suggest that p44/42 MAPK contributes to the up-regulation of caspase-3 mRNA and the JNK pathway regulates caspase-3 protein levels posttranslationally in -induced apoptosis in PC12 cells. |
1(0,0,0,1) | Details |
| 17382198 | Millar TM, Phan V, Tibbles LA: ROS generation in endothelial hypoxia and reoxygenation stimulates MAP kinase signaling and kinase-dependent neutrophil recruitment. Free Radic Biol Med. 2007 Apr 15;42(8):1165-77. Epub 2007 Jan 13. Endothelial cells exposed to relative hypoxia or the mitochondrial inhibitors rotenone, antimycin A, or FCCP show loss of mitochondrial membrane potential. Phosphorylation of stress-responsive mitogen-activated protein kinases occurred in hypoxia and was rapid and prolonged. |
2(0,0,0,2) | Details |
| 18373731 | Minelli A, Conte C, Grottelli S, Bellezza M, Cacciatore I, Bolanos JP: Cyclo (His-Pro) promotes cytoprotection by activating Nrf2-mediated up-regulation of antioxidant defence. J Cell Mol Med. 2009 Jun;13(6):1149-61. Epub 2008 Mar 29. Cyclo (His-Pro) attenuated reactive species production, and prevented depletion caused by rotenone, paraquat and beta-amyloid treatment. Finally, pharmacological inhibition of p-38 MAPK partially prevented both cyclo (His-Pro)-mediated Nrf2 activation and cellular protection. |
2(0,0,0,2) | Details |
| 14672949 | Sawada H, Kohno R, Kihara T, Izumi Y, Sakka N, Ibi M, Nakanishi M, Nakamizo T, Yamakawa K, Shibasaki H, Yamamoto N, Akaike A, Inden M, Kitamura Y, Taniguchi T, Shimohama S: Proteasome mediates dopaminergic neuronal degeneration, and its inhibition causes alpha-synuclein inclusions. J Biol Chem. 2004 Mar 12;279(11):10710-9. Epub 2003 Dec 12. Here we report that a combination of 1-methyl-4-phenylpyridinium ion (MPP (+)) or rotenone and proteasome inhibition causes the appearance of alpha-synuclein-positive inclusion bodies. MPP (+) elevated proteasome activity, dephosphorylated mitogen-activating protein kinase (MAPK), and activated caspase-3. |
2(0,0,0,2) | Details |
| 15843045 | Tomaselli B, Podhraski V, Heftberger V, Bock G, Baier-Bitterlich G: nucleoside-mediated protection of chemical hypoxia-induced neuronal injuries involves p42/44 MAPK activation. Neurochem Int. 2005 Jun;46(7):513-21. O (2)-sensitive neuronal pheochromocytoma (PC12)-cells, which are widely used as a model system for sympathetic ganglion-like neurons, were subjected to chemical hypoxia induced with rotenone, an inhibitor of mitochondrial complex I. |
2(0,0,0,2) | Details |
| 19131585 | Han Z, Varadharaj S, Giedt RJ, Zweier JL, Szeto HH, Alevriadou BR: Mitochondria-derived reactive species mediate heme oxygenase-1 expression in sheared endothelial cells. J Pharmacol Exp Ther. 2009 Apr;329(1):94-101. Epub 2009 Jan 8. Either phosphatidylinositol 3-kinase or mitogen-activated protein kinase cascade inhibitors blocked the HO-1 induction. The mitochondrial electron transport chain inhibitors, myxothiazol, rotenone, or antimycin A, and the mitochondria-targeted antioxidant peptide, Szeto-Schiller (SS)-31, which scavenges O (2)(*-), peroxide (H (2) O (2)), and markedly inhibited the increase in HO-1 expression. |
1(0,0,0,1) | Details |
| 19088429 | Oliver R 3rd, Friday E, Turturro F, Welbourne T: Troglitazone induced cytosolic acidification via extracellular signal-response kinase activation and mitochondrial depolarization: complex I pumping regulates ammoniagenesis in proximal tubule-like LLC-PK1 cells. Cell Physiol Biochem. 2008;22(5-6):475-86. Epub 2008 Dec 9. TRO-enhanced acid production was correlated with mitochondrial membrane potential and rotenone and 5-(N-ethyl-N-isopropyl) amiloride, were employed to test specifically the role of Complex I pumping. Preventing TRO-induced Extracellular Signal-Regulated Kinase activation with Mitogen Activated Protein Kinase Kinase inhibitors blocked the increase in acid production, restored /hydrogen ion exchanger-activity and prevented cytosolic acidification. |
1(0,0,0,1) | Details |
| 12003789 | Kulisz A, Chen N, Chandel NS, Shao Z, Schumacker PT: Mitochondrial ROS initiate phosphorylation of p38 MAP kinase during hypoxia in cardiomyocytes. Am J Physiol Lung Cell Mol Physiol. 2002 Jun;282(6):L1324-9. The p38 mitogen-activated protein kinase (MAPK) is phosphorylated in response to oxidative stress. This response was inhibited by rotenone, thenoyltrifluoroacetone, and myxothiazol, inhibitors of mitochondrial complexes I, II, and III, respectively. |
2(0,0,0,2) | Details |
| 15749729 | Simoncini S, Sapet C, Camoin-Jau L, Bardin N, Harle JR, Sampol J, Dignat-George F, Anfosso F: Role of reactive species and p38 MAPK in the induction of the pro-adhesive endothelial state mediated by IgG from patients with anti-phospholipid syndrome. Int Immunol. 2005 Apr;17(4):489-500. Epub 2005 Mar 4. ROS inhibition observed in the presence of diphenylene iodonium and rotenone indicated an involvement of a membrane-bound oxidase and the mitochondrial transport chain as sources of ROS. |
2(0,0,0,2) | Details |
| 16024921 | Yang T, Zhang A, Honeggar M, Kohan DE, Mizel D, Sanders K, Hoidal JR, Briggs JP, Schnermann JB: Hypertonic induction of COX-2 in collecting duct cells by reactive species of mitochondrial origin. J Biol Chem. 2005 Oct 14;280(41):34966-73. Epub 2005 Jul 17. Our previous studies have documented MAPK mediation of the hypertonicity-induced stimulation of COX-2 expression in cultured renal medullary epithelial cells. The increases in ROSs in response to hypertonic treatment were completely blocked by any one of the mitochondrial inhibitors tested, such as rotenone, thenoyltrifluoroacetone, or carbonyl m-chlorophenylhydrazone, associated with remarkable inhibition of COX-2 expression. |
1(0,0,0,1) | Details |
| 10900173 | Bogoyevitch MA, Ng DC, Court NW, Draper KA, Dhillon A, Abas L: Intact mitochondrial electron transport function is essential for signalling by peroxide in cardiac myocytes. J Mol Cell Cardiol. 2000 Aug;32(8):1469-80. A variety of inhibitors which act at different levels of the mitochondrial electron transport chain (rotenone, theonyltrifluoroacetone, antimycin A, also inhibited activation of the ERK MAPKs by peroxide but not TPA or hyperosmotic shock. Within 5 min, the ERK mitogen-activated protein kinases (ERK MAPKs) were activated. |
1(0,0,0,1) | Details |
| 15328001 | Alba G, El Bekay R, Alvarez-Maqueda M, Chacon P, Vega A, Monteseirin J, Santa Maria C, Pintado E, Bedoya FJ, Bartrons R, Sobrino F: Stimulators of AMP-activated protein kinase inhibit the respiratory burst in human neutrophils. FEBS Lett. 2004 Aug 27;573(1-3):219-25. Furthermore, also strongly reduced PMA-dependent H2O2 release, and induced the phosphorylation of c-jun N-terminal kinase 1 (p46), p38 mitogen-activated protein kinase and extracellular signal-regulated kinase. |
1(0,0,0,1) | Details |
| 16571865 | Li Z, Hyseni X, Carter JD, Soukup JM, Dailey LA, Huang YC: Pollutant particles enhanced H2O2 production from NAD (P) H oxidase and mitochondria in human pulmonary artery endothelial cells. Am J Physiol Cell Physiol. 2006 Aug;291(2):C357-65. Epub 2006 Mar 29. We hypothesized that PM enhanced oxidative stress in vascular endothelial cells and investigated the enzymatic sources of reactive species and their effects on mitogen-activated protein kinase (MAPK) activation and vasoconstriction. Inhibitors of other H2O2-producing enzymes, including Nomega-methyl-L-argnine, indomethacin, allopurinol, cimetidine, rotenone, and antimycin, had no effects. |
1(0,0,0,1) | Details |
| 19371610 | Mo Y, Wan R, Chien S, Tollerud DJ, Zhang Q: Activation of endothelial cells after exposure to ambient ultrafine particles: the role of oxidase. Toxicol Appl Pharmacol. 2009 Apr 15;236(2):183-93. Epub 2009 Feb 5. To investigate the activation of endothelial cells by UFP-induced oxidative stress, we determined the activation of the mitogen-activated protein kinases (MAPKs) in MPMVEC. Our results showed that UFPs, at a non-toxic dose, induced reactive species (ROS) generation in mouse pulmonary microvascular endothelial cells (MPMVEC) that was inhibited by pre-treatment with the ROS scavengers or inhibitors, but not with the mitochondrial inhibitor, rotenone. |
1(0,0,0,1) | Details |
| 19885011 | Kim HJ, Song JY, Park HJ, Park HK, Yun DH, Chung JH: Protects against Rotenone-induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells. Korean J Physiol Pharmacol. 2009 Aug;13(4):281-5. Epub 2009 Aug 31. We assessed cell death and apoptosis by measuring mitogen-activated protein kinase (MAPKs) and caspase (CASPs) activities and by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay, 4,6-diamidino-2-phenylindole (DAPI) staining, and terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) staining. |
1(0,0,0,1) | Details |
| 18563357 | Han M, Im DS: Effects of mitochondrial inhibitors on cell viability in U937 monocytes under deprivation. Arch Pharm Res. 2008 Jun;31(6):749-57. Epub 2008 Jun 19. Mitochondrial inhibitors such as rotenone, TTFA, antimycin A, azide, oligomycin, and valinomycin were used in this study. Activities of Akt and p38 MAPK, however, were decreased by the inhibitors under deprivation condition except TTFA. |
1(0,0,0,1) | Details |
| 12631583 | Schafer M, Ewald N, Schafer C, Stapler A, Piper HM, Noll T: Signaling of hypoxia-induced autonomous proliferation of endothelial cells. FASEB J. 2003 Mar;17(3):449-51. Epub 2003 Jan 21. In cultured endothelial cells of porcine aorta, we analyzed the signaling and compared hypoxia with mitochondrial inhibition by rotenone. Particularly, roles of the mitogen-activated protein kinase (MAPK) kinase (MEK)/MAPK pathway and cytosolic Ca2+ were studied. |
1(0,0,0,1) | Details |
| 16573651 | Casarejos MJ, Menendez J, Solano RM, Rodriguez-Navarro JA, Garcia de Yebenes J, Mena MA: Susceptibility to rotenone is increased in neurons from parkin null mice and is reduced by minocycline. J Neurochem. 2006 May;97(4):934-46. Epub 2006 Mar 29. The roles of p38 MAPK and extracellular signal-regulated kinase signaling pathways were tested by treatment with SB20358 and PD98059, respectively. |
1(0,0,0,1) | Details |
| 15170659 | Morazzani M, de Carvalho DD, Kovacic H, Smida-Rezgui S, Briand C, Penel C: Monolayer versus aggregate balance in survival process for EGF-induced apoptosis in A431 carcinoma cells: Implication of ROS-P38 MAPK-integrin alpha2beta1 pathway. Int J Cancer. 2004 Jul 20;110(6):788-99. EGF-induced dose-dependent ROS production was inhibited by the oxidase inhibitor, diphenylene iodonium (DPI), in these cells while rotenone was ineffective. |
1(0,0,0,1) | Details |
| 12591985 | Chun KH, Kosmeder JW 2nd, Sun S, Pezzuto JM, Lotan R, Hong WK, Lee HY: Effects of deguelin on the phosphatidylinositol 3-kinase/Akt pathway and apoptosis in premalignant human bronchial epithelial cells. J Natl Cancer Inst. 2003 Feb 19;95(4):291-302. The effects of deguelin on the phosphatidylinositol 3-kinase (PI3K)/Akt and mitogen-activated protein kinase (MAPK) pathways were assessed by western blot analyses and with adenoviral vectors that expressed constitutively active Akt. |
1(0,0,0,1) | Details |
| 17389326 | Chen YH, Lin SJ, Lin FY, Wu TC, Tsao CR, Huang PH, Liu PL, Chen YL, Chen JW: High glucose impairs early and late endothelial progenitor cells by modifying -related but not oxidative stress-mediated mechanisms. Diabetes. 2007 Jun;56(6):1559-68. Epub 2007 Mar 26. Antioxidants including -and polyethylene glycol (PEG)-conjugated superoxide dismutase, and PEG-catalase had no effects, whereas pyrrolidine dithiocarbamate, diphenyleneiodonium, apocynin, and rotenone even deteriorated the downregulation of both EPCs. |
0(0,0,0,0) | 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. |
0(0,0,0,0) | Details |
| 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). |
112(1,2,2,2) | Details |
| 15677311 | Rhyu DY, Yang Y, Ha H, Lee GT, Song JS, Uh ST, Lee HB: Role of reactive species in TGF-beta1-induced mitogen-activated protein kinase activation and epithelial-mesenchymal transition in renal tubular epithelial cells. J Am Soc Nephrol. 2005 Mar;16(3):667-75. Epub 2005 Jan 26. Growth-arrested and synchronized NRK-52E cells were stimulated with TGF-beta1 (0.2 to 20 ng/ml) or H (2) O (2) (1 to 500 microM) in the presence or absence of antioxidants or catalase), inhibitors of oxidase (diphenyleneiodonium and apocynin), mitochondrial electron transfer chain subunit I (rotenone), and MAPK (PD 98059, an MEK [MAP kinase/ERK kinase] inhibitor, or p38 MAPK inhibitor) for up to 96 h. |
85(1,1,1,5) | 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. |
81(1,1,1,1) | Details |
| 18705696 | Liu WH, Chang LS: Reactive species and p38 mitogen-activated protein kinase induce apoptotic death of U937 cells in response to Naja nigricollis toxin gamma. J Cell Mol Med. 2008 Aug 14. Noticeably, pretreatment with or rotenone eliminated markedly ROS accompanied with reduction in p38 MAPK activation. |
84(1,1,1,4) | Details |
| 20187293 | Liu WH, Chang LS: Reactive species and p38 mitogen-activated protein kinase induce apoptotic death of U937 cells in response to Naja nigricollis toxin-gamma. J Cell Mol Med. 2009 Aug;13(8B):1695-705. Noticeably, pre-treatment with or rotenone eliminated markedly ROS accompanied with reduction in p38 MAPK activation. |
84(1,1,1,4) | Details |
| 20157567 | Hsieh CC, Papaconstantinou J: Dermal fibroblasts from long-lived Ames dwarf mice maintain their in vivo resistance to mitochondrial generated reactive oxygen species (ROS). Aging (Albany NY). 2009 Jul 31;1(9):784-802. In these studies we demonstrate that dermal fibroblasts from these long-lived mice exhibit (a) higher levels of (SH)(2) Trx-ASK1 that correlate with their resistance to ROS generated by inhibitors of electron transport chain complexes CI (rotenone), CII (3-nitropropionic acid), CIII, (antimycin A), and H (2) O (2)-mediated activation of p38 MAPK, and (b) maintain their in vivo resistance to ROS generated by 3NPA. |
33(0,1,1,3) | 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 |
| 16819171 | Zhao FL, Hu JH, Zhu XZ: Monocyte-mediated rotenone neurotoxicity towards human neuroblastoma SH-SY5Y: role of mitogen-activated protein kinases. Biol Pharm Bull. 2006 Jul;29(7):1372-7. |
31(0,1,1,1) | 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. |
31(0,1,1,1) | Details |
| 19723537 | Park HJ, Kim HJ, Park HK, Chung JH: Protective effect of histamine H2 receptor antagonist against rotenone-induced apoptosis. Neurotoxicology. 2009 Nov;30(6):1114-9. Epub 2009 Aug 31. In this study, we investigated the protective effects of the H (2) receptor antagonist on rotenone-induced apoptosis in human dopaminergic SH-SY5Y cells, focusing on mitogen-activated protein kinases (MAPKs) and caspases (CASPs)-mediated apoptotic events. |
31(0,1,1,1) | Details |
| 12130563 | Hsieh TJ, Zhang SL, Filep JG, Tang SS, Ingelfinger JR, Chan JS: High glucose stimulates angiotensinogen gene expression via reactive species generation in rat kidney proximal tubular cells. Endocrinology. 2002 Aug;143(8):2975-85. The present studies investigated whether the effect of high levels on angiotensinogen (ANG) gene expression in kidney proximal tubular cells is mediated via reactive species (ROS) generation and p38 MAPK activation. These effects of high were blocked by antioxidants and tiron), inhibitors of mitochondrial electron transport chain complex I (rotenone) and II (thenoyltrifluoroacetone), an inhibitor of glycolysis-derived transport into mitochondria (alpha-cyano- an uncoupler of oxidative phosphorylation (carbonyl m-chlorophenylhydrazone), a manganese superoxide dismutase mimetic, catalase, and a specific inhibitor of p38 MAPK (SB 203580), but were not affected by an inhibitor of the - shuttle (aminooxyacetate acid). |
5(0,0,0,5) | Details |
| 19339632 | Huang S, Zhang A, Ding G, Chen R: -induced mesangial cell proliferation is mediated by EGF receptor transactivation. Am J Physiol Renal Physiol. 2009 Jun;296(6):F1323-33. Epub 2009 Apr 1. Pretreatment with the antioxidant N-acetyl- catalase, SOD, mitochondrial respiratory chain complex I inhibitor rotenone (Rot), oxidase inhibitor apocynin, and DPI significantly inhibited Aldo-stimulated MC proliferation as well as EGFR transactivation. Continuing our observations downstream in the signaling pathway, we examined the ability of Aldo to activate both the Ras/MAPK and the PI3K signaling pathways. |
4(0,0,0,4) | Details |
| 18840762 | Eley HL, Russell ST, Tisdale MJ: Mechanism of attenuation of muscle protein degradation induced by tumor necrosis factor-alpha and angiotensin II by Am J Physiol Endocrinol Metab. 2008 Dec;295(6):E1417-26. Epub 2008 Oct 7. Formation of ROS was attenuated by rotenone, an inhibitor of the mitochondrial electron transport chain, nitro- methyl ester, an inhibitor of synthase, and SB 203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), which also attenuated total protein degradation. Formation of ROS was attenuated by rotenone, an inhibitor of the mitochondrial electron transport chain, nitro- methyl ester, an inhibitor of synthase, and SB 203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), which also attenuated total protein degradation. |
3(0,0,0,3) | Details |
| 16778190 | Kim YM, Kim KE, Koh GY, Ho YS, Lee KJ: peroxide produced by angiopoietin-1 mediates angiogenesis. Cancer Res. 2006 Jun 15;66(12):6167-74. We found that human umbilical vein endothelial cells treated with Ang1 produce ROS transiently, which was suppressed by oxidase inhibitor, diphenylene-iodonium and rotenone. Removal of H2O2 by adenovirus-catalase significantly suppressed Ang1-induced in vitro endothelial cell migration, in vivo tubule formation and angiogenesis, and activation of p44/42 mitogen-activated protein kinase (MAPK), involved in cell migration, and delayed the deactivation of Akt phosphorylation involved in cell survival. |
2(0,0,0,2) | Details |
| 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. The selective ability of paraquat and rotenone to induce apoptosis in different cell lines correlates with their ability to activate c-Jun N-terminal protein kinase (JNK) and p38 mitogen-activated protein kinases. |
31(0,1,1,1) | 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). |
31(0,1,1,1) | Details |
| 12388366 | Parinandi NL, Kleinberg MA, Usatyuk PV, Cummings RJ, Pennathur A, Cardounel AJ, Zweier JL, Garcia JG, Natarajan V: Hyperoxia-induced NAD (P) H oxidase activation and regulation by MAP kinases in human lung endothelial cells. Am J Physiol Lung Cell Mol Physiol. 2003 Jan;284(1):L26-38. Epub 2002 Jul 26. Exposure of HPAECs to hyperoxia for 1, 3, and 12 h increased the generation of which was blocked by diphenyleneiodonium but not by rotenone or Exposure of HPAECs to hyperoxia activated p38 MAPK and ERK, and inhibition of p38 MAPK and MEK1/2 attenuated the hyperoxia-induced ROS generation. |
2(0,0,0,2) | Details |
| 15650392 | Bundy RE, Hoare GS, Kite A, Beach J, Yacoub M, Marczin N: Redox regulation of p38 MAPK activation and expression of ICAM-1 and heme oxygenase-1 in human alveolar epithelial (A549) cells. Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):14-24. The mitochondrial complex I and III inhibitors, rotenone and antimycin A, and allopurinol partially inhibited H2O2- but not TNFalpha-induced p38 activation. |
2(0,0,0,2) | Details |
| 16413574 | Zhang C, Hein TW, Wang W, Ren Y, Shipley RD, Kuo L: Activation of JNK and xanthine oxidase by TNF-alpha impairs -mediated dilation of coronary arterioles. J Mol Cell Cardiol. 2006 Feb;40(2):247-57. Epub 2006 Jan 18. Conversely, the effects of TNF were insensitive to inhibitors of p38 (SB203580), ERK (PD98059), NAD (P) H oxidase (apocynin), or mitochondrial respiratory chain (rotenone). Herein, we examined whether TNF can affect endothelium-dependent (NO)-mediated dilation of coronary arterioles to and whether inflammatory signaling pathways such as mitogen-activated protein kinases, sphingolipids, and oxidative stress are involved in the TNF-mediated effect. |
1(0,0,0,1) | Details |
| 15778391 | Sim S, Yong TS, Park SJ, Im KI, Kong Y, Ryu JS, Min DY, Shin MH: oxidase-derived reactive species-mediated activation of ERK1/2 is required for apoptosis of human neutrophils induced by Entamoeba histolytica. J Immunol. 2005 Apr 1;174(7):4279-88. However, a mitochondrial inhibitor rotenone did not attenuate the Entamoeba-induced ROS generation and apoptosis. Although E. histolytica strongly induced activation of ERK1/2 and p38 MAPK in neutrophils, the activation of ERK1/2 was closely associated with ROS-mediated apoptosis. |
1(0,0,0,1) | Details |
| 19074146 | Ren Y, Jiang H, Yang F, Nakaso K, Feng J: Parkin protects dopaminergic neurons against microtubule-depolymerizing toxins by attenuating microtubule-associated protein kinase activation. J Biol Chem. 2009 Feb 6;284(6):4009-17. Epub 2008 Dec 11. Mitogen-activated protein kinases, originally known as microtubule-associated protein (MAP) kinases, are activated in response to a variety of stimuli. Such mutations produced truncated parkin proteins lacking any microtubule binding domain and prevented parkin from protecting midbrain dopaminergic neurons against microtubule-depolymerizing toxins such as rotenone or colchicine. |
1(0,0,0,1) | Details |
| 16449798 | Hsieh CC, Papaconstantinou J: Thioredoxin-ASK1 complex levels regulate ROS-mediated p38 MAPK pathway activity in livers of aged and long-lived Snell dwarf mice. FASEB J. 2006 Feb;20(2):259-68. We have proposed that the age-associated increase of reactive species (ROS) by electron transport chain (ETC) dysfunction may cause the elevated basal level of p38 MAPK stress response pathway activity. Here we propose that activation of the p38 MAPK pathway by complex I (CI) generated ROS, in response to rotenone (ROT) treatment, is based on the ability of reduced Trx to bind to and inhibit ASK 1 and its release from the complex upon oxidation. |
1(0,0,0,1) | Details |
| 15863496 | Taille C, El-Benna J, Lanone S, Boczkowski J, Motterlini R: Mitochondrial respiratory chain and NAD (P) H oxidase are targets for the antiproliferative effect of in human airway smooth muscle. J Biol Chem. 2005 Jul 8;280(27):25350-60. Epub 2005 Apr 29. Here we show that a recently identified -releasing molecule, [Ru (CO) 3Cl2] 2 (or CORM-2) 1) inhibits NAD (P) H oxidase cytochrome b558 activity, 2) increases oxidant production by the mitochondria, and 3) inhibits ASMC proliferation and phosphorylation of the ERK1/2 mitogen-activated protein kinase and expression of cyclin D1, two critical pathways involved in muscle proliferation. Because both diphenylene iodinium or apocynin (inhibitors of NAD (P) H oxidase) and rotenone (a molecule that increases mitochondrial ROS production by blocking the respiratory chain) mimicked the effect of CORM-2 on cyclin D1 expression and ASMC proliferation, the antiproliferative effect of CORM-2 is probably related to inhibition of cytochromes on both NAD (P) H oxidase and the respiratory chain. |
1(0,0,0,1) | Details |