| Name | ERK1 |
|---|---|
| Synonyms | ERK 1; ERK1; ERT 2; ERT2; Extracellular signal regulated kinase 1; Extracellular signal related kinase 1b; Extracellular signal related kinase 1c; HS44KDAP… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16641227 | Hsuan SL, Klintworth HM, Xia Z: Basic fibroblast growth factor protects against rotenone-induced dopaminergic cell death through activation of extracellular signal-regulated kinases 1/2 and phosphatidylinositol-3 kinase pathways. J Neurosci. 2006 Apr 26;26(17):4481-91. Here we report that rotenone-induced apoptosis in human dopaminergic SH-SY5Y cells is attenuated by pretreatment with several growth factors, most notably basic fibroblast growth factor (bFGF). bFGF activated both extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase (PI3-kinase) pathways in SH-SY5Y cells. |
244(3,3,3,4) | Details |
| 16818739 | Yi JS, Holbrook BC, Michalek RD, Laniewski NG, Grayson JM: Electron transport complex I is required for CD8+ T cell function. . J Immunol. 2006 Jul 15;177(2):852-62. Within minutes of T cell activation, rotenone incubation decreased the production of H (2) O (2), flux, and ERK1/2 phosphorylation. |
81(1,1,1,1) | 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. peroxide-triggered activation of caspase-3 and ERK1/2 was attenuated by pretreatment with rotenone. |
34(0,1,1,4) | Details |
| 17596522 | Zhang A, Jia Z, Guo X, Yang T: induces epithelial-mesenchymal transition via ROS of mitochondrial origin. Am J Physiol Renal Physiol. 2007 Sep;293(3):F723-31. Epub 2007 Jun 27. Aldo induced phosphorylation of ERK1/2 that was completely blocked by rotenone. |
32(0,1,1,2) | 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). |
31(0,1,1,1) | Details |
| 18452993 | Cho HS, Kim S, Lee SY, Park JA, Kim SJ, Chun HS: Protective effect of the green tea component, L-theanine on environmental toxins-induced neuronal cell death. Neurotoxicology. 2008 Jul;29(4):656-62. Epub 2008 Mar 20. Both rotenone- and dieldrin-induced down-regulation of extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylation was significantly blocked by pretreatment with L-theanine. |
31(0,1,1,1) | 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. |
31(0,1,1,1) | 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. (Aldo) stimulates glomerular mesangial cell (MC) proliferation, in part, through an ERK1/2-dependent pathway. |
3(0,0,0,3) | 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. |
3(0,0,0,3) | 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. Our results showed that exposure of MPMVEC to UFPs caused increased phosphorylation of p38 and ERK1/2 MAPKs that was blocked by pre-treatment with DPI or p67 (phox) siRNA. 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. |
2(0,0,0,2) | 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. (CO), one of the end products of heme oxygenase activity, inhibits smooth muscle proliferation by decreasing ERK1/2 phosphorylation and cyclin D1 expression, a signaling pathway that is known to be modulated by reactive species (ROS) in airway smooth muscle cells (ASMCs). 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. |
2(0,0,0,2) | Details |
| 16378625 | Wu CC, Hsu MC, Hsieh CW, Lin JB, Lai PH, Wung BS: Upregulation of heme oxygenase-1 by via the phosphatidylinositol 3-kinase/Akt and ERK pathways. Life Sci. 2006 May 15;78(25):2889-97. Epub 2005 Dec 27. The inhibition of intracellular ROS production by (NAC), (GSH), superoxide dismutase (SOD), catalase and the mitochondrial complex I inhibitor, rotenone, results in a decrease in -dependent HO-1 expression. ECs treated with exhibit activation of Akt and ERK1/2. |
2(0,0,0,2) | 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 measured the production of extracellular H2O2, activation of extracellular signal-regulated kinases1/2 (ERK1/2) and p38 MAPKs in human pulmonary artery endothelial cells (HPAEC) treated with urban particles (UP; SRM1648), and assessed the effects of H2O2 on vasoconstriction in pulmonary artery ring and isolated perfused lung. Inhibitors of other H2O2-producing enzymes, including Nomega-methyl-L-argnine, indomethacin, allopurinol, cimetidine, rotenone, and antimycin, had no effects. |
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. Proteasome inhibition reversed the MAPK dephosphorylation and blocked caspase-3 activation; the neuroprotection was blocked by a p42 and p44 MAPK kinase inhibitor. |
1(0,0,0,1) | Details |
| 18801963 | Garciarena CD, Caldiz CI, Correa MV, Schinella GR, Mosca SM, Chiappe de Cingolani GE, Cingolani HE, Ennis IL: Na+/H+ exchanger-1 inhibitors decrease myocardial production via direct mitochondrial action. J Appl Physiol. 2008 Dec;105(6):1706-13. Epub 2008 Sep 18. The mitochondria appeared to be the source of the NOX-dependent ROS released by the "ROS-induced ROS release mechanism" that was blunted by the mitochondrial ATP-sensitive potassium channel blockers 5-hydroxydecanoate and glibenclamide, inhibition of complex I of the electron transport chain with rotenone, and inhibition of the permeability transition pore (MPTP) by cyclosporin A. Increased O (2)(-) production, as expected, stimulated ERK1/2 and p90 ribosomal S6 kinase phosphorylation. |
1(0,0,0,1) | Details |
| 20231142 | Villa-Abrille MC, Caldiz CI, Ennis IL, Nolly MB, Casarini MJ, Chiappe de Cingolani GE, Cingolani HE, Perez NG: The Anrep effect requires transactivation of the epidermal growth factor receptor. J Physiol. 2010 Mar 15. Stretch increased ERK1/2 phosphorylation by 196+/-17% of control, n=7 (P <0.05), effect that was prevented by PPI (124+/-22%, n=7) and AG1478 (131+/-17%, n=4). EGF increased O2- production by 149+/-4% of control (n=9, P <0.05), effect canceled by inhibiting oxidase (apocynin, 110+/-6% n=7), mKATP channels (5-HD, 105+/-5%, n=8), respiratory chain (rotenone, 110+/-7%, n=7) or MPTP (Cyclosporine, 111+/-10%, n=6). |
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. The increases in phosphorylation of ERK1/2 and p38 were detected 20 min following the hypertonic treatment and were both prevented by N-acetyl- 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 |
| 15111505 | Ceolotto G, Bevilacqua M, Papparella I, Baritono E, Franco L, Corvaja C, Mazzoni M, Semplicini A, Avogaro A: Insulin generates free radicals by an NAD (P) H, phosphatidylinositol 3'-kinase-dependent mechanism in human skin fibroblasts ex vivo. Diabetes. 2004 May;53(5):1344-51. Therefore, we examined whether acute hyperinsulinemia increases the production of free radicals and whether this condition affects proliferative extracellular signal-regulated kinase (ERK-1 and -2) signaling in human fibroblasts in vitro. Furthermore, insulin-induced O (2)(-) production was attenuated by the NAD (P) H inhibitor apocynin, but not by rotenone or |
1(0,0,0,1) | Details |
| 17047462 | Kim SJ, Kim JS, Cho HS, Lee HJ, Kim SY, Kim S, Lee SY, Chun HS: a component of rosemary (Rosmarinus officinalis L.) protects nigral dopaminergic neuronal cells. Neuroreport. 2006 Nov 6;17(16):1729-33. In this study, we investigated the protective effects of on rotenone-induced neurotoxicity in cultured dopaminergic cells. Furthermore, significantly increased the tyrosine hydroxylase, Nurr1, and extracellular signal-regulated kinase 1/2. |
1(0,0,0,1) | Details |
| 19857556 | Li X, Liu Z, Tamashiro K, Shi B, Rudnicki DD, Ross CA, Moran TH, Smith WW: Synphilin-1 exhibits trophic and protective effects against Rotenone toxicity. Neuroscience. 2010 Jan 20;165(2):455-62. Epub . We further found that synphilin-1 increased activation of the extracellular signal-regulated kinases (ERK1/2) and mediated neurite outgrowth. |
1(0,0,0,1) | Details |