| Name | phosphatidylinositol 3 kinase (protein family or complex) |
|---|---|
| Synonyms | PI3 kinase; PI3 kinases; PI3K; Phosphatidylinositol 3 kinase; Phosphatidylinositol 3 kinases; Phosphatidylinositol 4,5 bisphosphate 3 kinase; Phosphatidylinositol 4,5 bisphosphate 3 kinases |
| 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. |
225(2,4,4,5) | Details |
| 17481595 | Hu JH, Zhu XZ: Rotenone-induced neurotoxicity of THP-1 cells requires production of reactive species and activation of phosphatidylinositol 3-kinase. Brain Res. 2007 Jun 11;1153:12-9. Epub 2007 Mar 12. |
112(1,2,2,2) | 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. Furthermore, insulin-induced O (2)(-) production was attenuated by the NAD (P) H inhibitor apocynin, but not by rotenone or |
2(0,0,0,2) | 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. |
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. |
2(0,0,0,2) | Details |
| 17885094 | Canas N, Valero T, Villarroya M, Montell E, Verges J, Garcia AG, Lopez MG: protects SH-SY5Y cells from oxidative stress by inducing heme oxygenase-1 via phosphatidylinositol 3-kinase/Akt. J Pharmacol Exp Ther. 2007 Dec;323(3):946-53. Epub 2007 Sep 20. Cell death caused by a combination of 10 microM rotenone plus 1 microM oligomycin-A (Rot/oligo) was also reduced by CS at concentrations ranging from 0.3 to 100 microM; in this toxicity model, maximum protection was achieved at 3 microM (48%). |
2(0,0,0,2) | Details |
| 11368352 | Salsman S, Felts N, Pye QN, Floyd RA, Hensley K: Induction of Akt phosphorylation in rat primary astrocytes by H2O2 occurs upstream of phosphatidylinositol 3-kinase: no evidence for oxidative inhibition of PTEN. Arch Biochem Biophys. 2001 Feb 15;386(2):275-80. Treatment with rotenone or antimycin A also resulted in increased wortmannin-sensitive Akt phosphorylation, probably by increasing intracellular H2O2 generation by blocking mitochondrial electron transport. These results suggest that activation of Akt by H2O2 occurs upstream of phosphatidylinositol 3-kinase (PI 3-K) activity in astrocytes. |
1(0,0,0,1) | 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 |
| 19252273 | Shimohama S: Nicotinic receptor-mediated neuroprotection in neurodegenerative disease models. Biol Pharm Bull. 2009 Mar;32(3):332-6. -induced protection was blocked by an alpha7 nAChR antagonist, a phosphatidylinositol 3-kinase (PI3K) inhibitor, and an Src inhibitor. Up-regulation of Bcl-2 and Bcl-x could prevent cells from neuronal death induced by beta-amyloid (Abeta), and rotenone. |
1(0,0,0,1) | Details |
| 12591974 | Crowell JA, Steele VE: AKT and the phosphatidylinositol 3-kinase/AKT pathway: important molecular targets for lung cancer prevention and treatment. J Natl Cancer Inst. 2003 Feb 19;95(4):252-3. |
1(0,0,0,1) | Details |
| 17634444 | Li Y, Chandrakanthan V, Day ML, O'Neill C: Direct evidence for the action of phosphatidylinositol (3,4,5)-trisphosphate-mediated signal transduction in the 2-cell mouse embryo. Biol Reprod. 2007 Nov;77(5):813-21. Epub 2007 Jul 18. Inhibitors of 1-o-phosphatidylinositol-3-kinase (PI3kinase), such as wortmannin and LY 294002, blocked these transients, implicating the generation of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) in autocrine signal transduction in the early embryo. |
1(0,0,0,1) | Details |
| 17360324 | Liu Y, Kern JT, Walker JR, Johnson JA, Schultz PG, Luesch H: A genomic screen for activators of the antioxidant response element. Proc Natl Acad Sci U S A. 2007 Mar 20;104(12):5205-10. Epub 2007 Mar 12. Studies with pharmacological inhibitors indicated that 1-phosphatidylinositol 3-kinase and protein kinase C signaling are essential for activity. Overexpression of these cDNAs conferred partial resistance to peroxide or rotenone-induced toxicity, consistent with the induction of antioxidant and phase II detoxification enzymes, which can protect from oxidative stress. |
1(0,0,0,1) | Details |
| 15486067 | Kim JH, Chu SC, Gramlich JL, Pride YB, Babendreier E, Chauhan D, Salgia R, Podar K, Griffin JD, Sattler M: Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive species. Blood. 2005 Feb 15;105(4):1717-23. Epub 2004 Oct 14. Elevated ROS levels in BCR-ABL-transformed cells were found to be blocked by the mitochondrial complex I inhibitor rotenone as well as the transport inhibitor suggesting that the source of increased ROS might be related to increased metabolism. metabolism in BCR-ABL-transformed cells is likely to be mediated by activation of the phosphatidylinositol-3'-kinase (PI3K) pathway, which is regulated through this site. |
1(0,0,0,1) | Details |
| 15313408 | Lee HY: Molecular mechanisms of deguelin-induced apoptosis in transformed human bronchial epithelial cells. Biochem Pharmacol. 2004 Sep 15;68(6):1119-24. Increasing evidence has demonstrated that the phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway plays an important role in cell proliferation, apoptosis, angiogenesis, adhesion, invasion, and migration, functions that are critical to cancer cell survival and metastasis. |
1(0,0,0,1) | 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 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. Additionally, Akt, p70 ribosomal protein S6 kinase, and S6 ribosomal protein were also phosphorylated upon sPLA (2)-IIA treatment, effect that was abrogated by or LY294002 treatment indicating that ROS and phosphatidylinositol 3 kinase are upstream signaling regulators. |
1(0,0,0,1) | Details |
| 16887804 | Jiang Q, Yan Z, Feng J: Neurotrophic factors stabilize microtubules and protect against rotenone toxicity on dopaminergic neurons. J Biol Chem. 2006 Sep 29;281(39):29391-400. Epub 2006 Aug 3. The protective effect of NGF was completely abolished by inhibiting the microtubule-associated protein kinase kinase (MEK) and partially reversed by blocking phosphatidylinositol 3-kinase. |
1(0,0,0,1) | Details |
| 18593368 | Yi T, Li H, Wang X, Wu Z: Enhancement radiosensitization of breast cancer cells by deguelin. Cancer Biother Radiopharm. 2008 Jun;23(3):355-62. OBJECTIVE: Radiation can activate the phosphatidylinositol 3-kinase/Akt pathway and cannot downregulate survivin expression in breast cancer cells. |
1(0,0,0,1) | Details |
| 11689167 | King TD, Bijur GN, Jope RS: Caspase-3 activation induced by inhibition of mitochondrial complex I is facilitated by glycogen synthase kinase-3beta and attenuated by lithium. Brain Res. 2001 Nov 16;919(1):106-14. To test if the activation state of the cell survival-promoting phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway affects MPP-induced caspase-3 activation, PI3K was inhibited with LY294002, or activated with insulin-like growth factor-1. To test if these regulatory interactions applied to other mitochondrial complex I inhibitors, cells were treated with rotenone. |
1(0,0,0,1) | Details |
| 14871987 | Lee HY, Suh YA, Kosmeder JW, Pezzuto JM, Hong WK, Kurie JM: Deguelin-induced inhibition of cyclooxygenase-2 expression in human bronchial epithelial cells. Clin Cancer Res. 2004 Feb 1;10(3):1074-9. We demonstrated previously that deguelin inhibits proliferation of premalignant human bronchial epithelial (HBE) cells, such as 1799 cells and squamous HBE cells, by regulating phosphatidylinositol-3-kinase Akt activity, which is involved in COX-2 expression. |
1(0,0,0,1) | 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. Both rotenone and are possible neurotoxins for a wide variety of cell and neuronal types including dopaminergic neurons and induce apoptosis in various cells. |
0(0,0,0,0) | 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 |