| Name | caspase (protein family or complex) |
|---|---|
| Synonyms | caspase; caspases |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. Activation of ERK1/2 MAPK and caspases was assessed by Western blotting. Eosinophils were pretreated with rotenone, an inhibitor of the mitochondrial electron transport chain, before H2O2 was added. |
2(0,0,0,2) | 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. After treatment of deguelin (10 nM) combined with radiation (3 Gy), caspase-dependent apoptosis was significantly increased and cell cycle was arrested in the G2-M phase in MDA-MB-231 cells. |
2(0,0,0,2) | 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 |
| 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, 15dPG-J2 can also activate an intrinsic apoptotic pathway involving phosphatidyl serine externalization, caspase activation and cytochrome c release. 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. |
2(0,0,0,2) | Details |
| 11097871 | Gennari A, Viviani B, Galli CL, Marinovich M, Pieters R, Corsini E: Organotins induce apoptosis by disturbance of [Ca (2+)](i) and mitochondrial activity, causing oxidative stress and activation of caspases in rat thymocytes. Toxicol Appl Pharmacol. 2000 Dec 1;169(2):185-90. ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular Ca (2+) chelator, or rotenone, an inhibitor of the electron entry from complex I to indicating the important role of Ca (2+) and mitochondria during these early intracellular events. |
2(0,0,0,2) | Details |
| 16749863 | Souid AK, Penefsky HS, Sadowitz PD, Toms B: Enhanced cellular respiration in cells exposed to doxorubicin. . Mol Pharm. 2006 May-Jun;3(3):307-21. The increment in consumption was blocked by the pan-caspase inhibitor benzyloxycarbonyl-Val--dl-Asp-fluoromethylketone (zVAD-fmk) and by the PTP inhibitor cyclosporin A. The conclusion that both of the latter processes were products of oxidations in the mitochondrial respiratory chain was supported by the further observation that rotenone and inhibited consumption and substantially lowered ATP content in the treated and untreated cells. |
1(0,0,0,1) | Details |
| 12730670 | Djavaheri-Mergny M, Wietzerbin J, Besancon F: induces apoptosis in Ewing sarcoma cells through mitochondrial peroxide production. Oncogene. 2003 May 1;22(17):2558-67. Here, we report that 2-methoxy- (2-Me), a natural metabolite, induced a caspase-dependent apoptosis of Ewing sarcoma-derived cells independently of their p53 status. 2-Me-induced apoptosis occurred through the mitochondrial death pathway as evidenced by reduction of the mitochondrial transmembrane potential, cytochrome c release and caspase-9 activation. Rotenone, an inhibitor of the mitochondrial respiratory chain, abolished both apoptosis and H (2) O (2) production, thereby identifying mitochondria as the source of H (2) O (2). |
1(0,0,0,1) | 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. Inhibitors of electron transport (rotenone and antimycin A) or inhibitor of mitochondrial permeability transition pore (cyclosporine A) reduced the effect of toxin gamma on ROS generation, loss of DeltaPsim and cytochrome c release. Taken together, these results suggest that the cytotoxicity of toxin gamma is initiated by p38 MAPK-mediated mitochondrial dysfunction followed by ROS production and activation of caspases, and that ROS further augments p38 MAPK activation and mitochondrial alteration. |
1(0,0,0,1) | Details |
| 12782307 | Potokar M, Milisav I, Kreft M, Stenovec M, Zorec R: Apoptosis triggered redistribution of caspase-9 from cytoplasm to mitochondria. FEBS Lett. 2003 Jun 5;544(1-3):153-9. The activation of apoptosis with rotenone triggers the redistribution of caspase-9 to mitochondria. Experiments using the general caspase inhibitor z-VAD.fmk and the specific caspase-9 inhibitor z-LEHD.fmk show that the caspase-9 redistribution is a regulated process and requires the activity of a caspase other than the caspase-9. |
1(0,0,0,1) | Details |
| 17477947 | Hansen T, Seidel A, Borlak J: The environmental carcinogen 3-nitrobenzanthrone and its main metabolite 3-aminobenzanthrone enhance formation of reactive intermediates in human A549 lung epithelial cells. Toxicol Appl Pharmacol. 2007 Jun 1;221(2):222-34. Epub 2007 Mar 23. Mitochondrial ROS production was significantly attenuated (20% reduction) by addition of rotenone (complex I inhibition) and thenoyltrifluoroacetone (TTFA, complex II inhibition). Increased intracellular Ca (2+) and caspase activities were detected upon 3-NBA exposure. |
1(0,0,0,1) | Details |
| 17435593 | Lim ML, Mercer LD, Nagley P, Beart PM: Rotenone and MPP+ preferentially redistribute apoptosis-inducing factor in apoptotic neurons. Neuroreport. 2007 Mar 5;18(4):307-12. Preferential redistribution of apoptosis-inducing factor before cytochrome c in neurons indicates caspase-independent mitochondrial proapoptotic signalling predominates in these parkinsonian models. |
1(0,0,0,1) | Details |
| 10567579 | Li L, Lorenzo PS, Bogi K, Blumberg PM, Yuspa SH: Protein kinase Cdelta targets mitochondria, alters mitochondrial membrane potential, and induces apoptosis in normal and neoplastic keratinocytes when overexpressed by an adenoviral vector. Mol Cell Biol. 1999 Dec;19(12):8547-58. Mitochondrial inhibitors, rotenone and antimycin A, reduced TPA-induced cell death in PKCdelta-overexpressing keratinocytes. TPA-induced cell death was apoptotic as evidenced by morphological criteria, TUNEL (terminal deoxynucleotidyltransferase-mediated - nick end labeling) assay, DNA fragmentation, and increased caspase activity. |
1(0,0,0,1) | Details |
| 11078377 | Kakinuma Y, Miyauchi T, Yuki K, Murakoshi N, Goto K, Yamaguchi I: Mitochondrial dysfunction of cardiomyocytes causing impairment of cellular energy metabolism induces apoptosis, and concomitant increase in cardiac endothelin-1 expression. J Cardiovasc Pharmacol. 2000 Nov;36(5 Suppl 1):S201-4. In this study, we applied mitochondrial inhibitors, such as rotenone, and antimycin A, which inhibit mitochondrial function at different sites of the mitochondrial respiratory chain, to cardiomyocytes. It was shown that after 48-72 h of treatment with each reagent, apoptosis was shown to occur by DNA laddering and increase in caspase activity. |
1(0,0,0,1) | Details |
| 11229440 | Goossens V, Stange G, Moens K, Pipeleers D, Grooten J: Regulation of tumor necrosis factor-induced, mitochondria- and reactive species-dependent cell death by the electron flux through the electron transport chain complex I. Antioxid Redox Signal. 1999 Fall;1(3):285-95. Tumor necrosis factor (TNF) induces a caspase-independent but mitochondria-dependent cell death process in the mouse fibrosarcoma cell line L929. |
1(0,0,0,1) | Details |
| 19072121 | Thompson CM, Quinn CA, Hergenrother PJ: Total synthesis and cytoprotective properties of dykellic acid. J Med Chem. 2009 Jan 8;52(1):117-25. Many compounds that delay or prevent apoptotic death either reduce the amount of cellular reactive species (ROS) or are direct inhibitors of caspases. We have found that dykellic acid protects cells from death as induced by etoposide and rotenone. |
1(0,0,0,1) | Details |
| 17343987 | Alvira D, Tajes M, Verdaguer E, de Arriba SG, Allgaier C, Matute C, Trullas R, Jimenez A, Pallas M, Camins A: Inhibition of cyclin-dependent kinases is neuroprotective in 1-methyl-4-phenylpyridinium-induced apoptosis in neurons. Neuroscience. 2007 Apr 25;146(1):350-65. Epub 2007 Mar 7. In the present study, we examine the role of caspase-dependent and -independent routes in MPP+-induced apoptosis in rat cerebellar granule neurons (CGNs). |
1(0,0,0,1) | Details |
| 17227556 | Armann B, Hanson MS, Hatch E, Steffen A, Fernandez LA: Quantification of basal and stimulated ROS levels as predictors of islet potency and function. Am J Transplant. 2007 Jan;7(1):38-47. Also, flow cytometric analyses of ROS (dihydroethidine), apoptosis (Annexin V, active caspases), necrosis (Topro3), and mitochondrial membrane potential (JC-1) were done in parallel to correlate with changes in luminol-measured ROS. The ROS indices following and rotenone exposure are indicative of metabolic potency and mitochondrial integrity and can be used as surrogate markers to evaluate the quality of islets prior to transplantation. |
1(0,0,0,1) | Details |
| 18466357 | Castera L, Hatzfeld-Charbonnier AS, Ballot C, Charbonnel F, Dhuiege E, Velu T, Formstecher P, Mortier L, Marchetti P: Apoptosis-related mitochondrial dysfunction defines human monocyte-derived dendritic cells with impaired immuno-stimulatory capacities. J Cell Mol Med. 2009 Jul;13(7):1321-35. Epub 2008 May 3. Here, we report that cultured mature monocyte-derived DCs manifest early mitochondrial damage (i.e. within 24 hrs), characterized by mitochondrial membrane potential (psi Delta m) disruption and mitochondrial release of pro-apoptotic factors, followed by reactive species (ROS) production and activation of caspases. Perturbations to mitochondrial respiration with rotenone identified the same modifications to DC immune functions. |
1(0,0,0,1) | Details |
| 16412576 | Chen MJ, Yap YW, Choy MS, Koh CH, Seet SJ, Duan W, Whiteman M, Cheung NS: Early induction of calpains in rotenone-mediated neuronal apoptosis. Neurosci Lett. 2006 Apr 10-17;397(1-2):69-73. Epub 2006 Jan 10. This study aims to establish for the first time, the time-point of calpain activation with respect to the caspase activation and the possibility of cell cycle re-entry in rotenone-mediated cell death. |
224(2,4,4,4) | 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. Neuronal death was mainly apoptotic and suppressible by the caspase inhibitor t-butoxycarbonyl-Asp (OMe)-fluoromethyl ketone (Boc-D-FMK). |
1(0,0,0,1) | Details |
| 10908611 | Luetjens CM, Bui NT, Sengpiel B, Munstermann G, Poppe M, Krohn AJ, Bauerbach E, Krieglstein J, Prehn JH: Delayed mitochondrial dysfunction in excitotoxic neuron death: cytochrome c release and a secondary increase in production. J Neurosci. 2000 Aug 1;20(15):5715-23. Treatment with staurosporine induced mitochondrial release of cytochrome c, caspase activation, and cell death in control and rho (-) cells. The secondary rise could be inhibited by the complex I inhibitor rotenone (in combination with oligomycin) and mimicked by the complex III inhibitor antimycin A. |
1(0,0,0,1) | Details |
| 12832841 | Kitamura Y, Inden M, Sanada H, Takata K, Taniguchi T, Shimohama S, Orii H, Mochii M, Agata K, Watanabe K: Inhibitory effects of antiparkinsonian drugs and caspase inhibitors in a parkinsonian flatworm model. J Pharmacol Sci. 2003 Jun;92(2):137-42. These results suggest that the degeneration of planarian dopaminergic system induced by rotenone or MPTP may be mediated through caspase-like activation. |
113(1,2,2,3) | Details |
| 12551850 | Pei W, Liou AK, Chen J: Two caspase-mediated apoptotic pathways induced by rotenone toxicity in cortical neuronal cells. FASEB J. 2003 Mar;17(3):520-2. Epub 2003 Jan 22. |
112(1,2,2,2) | Details |
| 12401552 | Kitamura Y, Inden M, Miyamura A, Kakimura J, Taniguchi T, Shimohama S: Possible involvement of both mitochondria- and endoplasmic reticulum-dependent caspase pathways in rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells. Neurosci Lett. 2002 Nov 15;333(1):25-8. These results suggest that rotenone may induce activation of both mitochondria- and endoplasmic reticulum-dependent caspases in human SH-SY5Y cells. |
87(1,1,2,2) | Details |
| 10987825 | Bal-Price A, Brown GC: -induced necrosis and apoptosis in PC12 cells mediated by mitochondria. J Neurochem. 2000 Oct;75(4):1455-64. A 24-h incubation of PC12 cells with NO donors (SNAP or NOC-18) or specific inhibitors of mitochondrial respiration (myxothiazol, rotenone, or azide), in the absence of caused total ATP depletion and resulted in 80-100% necrosis. The presence of apoptotic cells was prevented completely by benzyloxycarbonyl-Val--fluoromethyl ketone (a nonspecific caspase inhibitor), indicating that apoptosis was mediated by caspase activation. |
1(0,0,0,1) | Details |
| 19781773 | Ito S, Oyake T, Murai K, Ishida Y: Deguelin suppresses cell proliferation via the inhibition of survivin expression and STAT3 phosphorylation in HTLV-1-transformed T cells. Leuk Res. 2010 Mar;34(3):352-7. Epub 2009 Sep 24. We also observed the cleavage of caspase-3 and poly (ADP- polymerase (PARP) in deguelin-treated cells, indicating that deguelin induces caspase-dependent apoptosis in these cells. |
1(0,0,0,1) | Details |
| 17900545 | Chung WG, Miranda CL, Maier CS: potentiates the cytotoxicity of rotenone in neuroblastoma SH-SY5Y cells. Brain Res. 2007 Oct 24;1176:133-42. Epub 2007 Aug 22. The exacerbating effect of on rotenone toxicity may involve an apoptotic mechanism as shown by the enhancement of caspase-3 activity and activation of other caspases in rotenone-treated SH-SY5Y cells. |
81(1,1,1,1) | Details |
| 15698934 | Wang XJ, Xu JX: Possible involvement of Ca2+ signaling in rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells. Neurosci Lett. 2005 Mar 11;376(2):127-32. Epub 2004 Dec 9. Notably, Ca2+ suppression also prevented rotenone-induced apoptotic related events including reactive species production, G2/M cell cycle arrest and caspase activation, suggesting that Ca2+ signaling is upstream to these events. |
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. |
81(1,1,1,1) | Details |
| 15764812 | Singh SV, Srivastava SK, Choi S, Lew KL, Antosiewicz J, Xiao D, Zeng Y, Watkins SC, Johnson CS, Trump DL, Lee YJ, Xiao H, Herman-Antosiewicz A: -induced cell death in human prostate cancer cells is initiated by reactive species. J Biol Chem. 2005 May 20;280(20):19911-24. Epub 2005 Mar 11. In conclusion, the results of the present study indicate that SFN-induced apoptosis in prostate cancer cells is initiated by ROS generation and that both intrinsic and extrinsic caspase cascades contribute to the cell death caused by this highly promising cancer chemopreventive agent. The SFN-induced ROS generation was significantly attenuated on pretreatment with mitochondrial respiratory chain complex I inhibitors, including diphenyleneiodonium and rotenone. |
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. These results suggest that parkin protects against toxicity by decreasing oxidative stress and ensuing activation of apoptotic programs such as the JNK/caspase pathway. 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. |
1(0,0,0,1) | Details |
| 17690326 | Nutku-Bilir E, Hudson SA, Bochner BS: Interleukin-5 priming of human eosinophils alters siglec-8 mediated apoptosis pathways. Am J Respir Cell Mol Biol. 2008 Jan;38(1):121-4. Epub 2007 Aug 9. Finally, both the mitochondrial electron transport inhibitor rotenone, and the ROS inhibitors diphenyleneiodonium and antimycin, completely inhibited Siglec-8-mediated apoptosis, even after IL-5 priming. These data demonstrate that IL-5 priming enhances Siglec-8-mediated mitochondrial and ROS-dependent eosinophil apoptosis and eliminates caspase dependence. |
1(0,0,0,1) | 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. Inhibitors of electron transport (rotenone and antimycin A) or inhibitor of mitochondrial permeability transition pore (cyclosporine A) reduced the effect of toxin- on ROS generation, loss of deltapsim and cytochrome c release. Taken together, these results suggest that the cytotoxicity of toxin- is initiated by p38-MAPK-mediated mitochondrial dysfunction followed by ROS production and activation of caspases, and that ROS further augments p38 MAPK activation and mitochondrial alteration. |
1(0,0,0,1) | Details |
| 15114628 | Shavali S, Carlson EC, Swinscoe JC, Ebadi M: a Parkinsonism-inducing endogenous toxin, increases alpha-synuclein expression and causes nuclear damage in human dopaminergic cells. J Neurosci Res. 2004 May 15;76(4):563-71. Inhibition of complex I by rotenone and depletion of by L-buthionine sulfoxamine also correlated with an increase in alpha-syn expression, suggesting that oxidative stress may cause an increase in alpha-syn levels in dopaminergic cells. The 1BnTIQ-induced alpha-syn up-regulation was inhibited by cotreatment with the antioxidants selegiline, (10), and N-acetylcystein and the caspase inhibitor DEVD-CHO. |
1(0,0,0,1) | Details |
| 12177198 | Sherer TB, Betarbet R, Stout AK, Lund S, Baptista M, Panov AV, Cookson MR, Greenamyre JT: An in vitro model of Parkinson's disease: linking mitochondrial impairment to altered alpha-synuclein metabolism and oxidative damage. J Neurosci. 2002 Aug 15;22(16):7006-15. In response to H2O2, there was cytochrome c release from mitochondria, caspase-3 activation, and apoptosis, all of which occurred earlier and to a much greater extent in rotenone-treated cells; caspase inhibition provided substantial protection. |
62(0,2,2,2) | Details |
| 12800192 | Weitsman GE, Ravid A, Liberman UA, Koren R: enhances caspase-dependent and -independent TNFalpha-induced breast cancer cell death: The role of reactive species and mitochondria. Int J Cancer. 2003 Aug 20;106(2):178-86. The effect of on DeltaPsi was mimicked by rotenone, which increased both the drop in DeltaPsi and caspase activation induced by TNFalpha. |
38(0,1,1,8) | Details |
| 12538580 | De Sarno P, Shestopal SA, King TD, Zmijewska A, Song L, Jope RS: Muscarinic receptor activation protects cells from apoptotic effects of DNA damage, oxidative stress, and mitochondrial inhibition. J Biol Chem. 2003 Mar 28;278(13):11086-93. Epub 2003 Jan 21. Oxotremorine-M pretreatment protected cells from H (2) O (2)-induced caspase-3 activation and death, and this was equivalent to protection afforded by a caspase inhibitor. Muscarinic receptor stimulation also protected cells from caspase-3 activation induced by exposure to rotenone, a mitochondrial complex 1 inhibitor, but no protection was evident from staurosporine-induced caspase-3 activation. |
1(0,0,0,1) | 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. These data suggest that rotenone induces apoptosis in the dopaminergic SH-SY5Y cells that requires activation of the JNK and p38 MAP kinases and caspases. |
37(0,1,2,2) | Details |
| 15806174 | Lee YJ, Lee DH, Cho CK, Chung HY, Bae S, Jhon GJ, Soh JW, Jeoung DI, Lee SJ, Lee YS: HSP25 inhibits radiation-induced apoptosis through reduction of PKCdelta-mediated ROS production. Oncogene. 2005 May 26;24(23):3715-25. In the present study, radiation-induced cytochrome c release from mitochondria and activation of caspases accompanied by a decrease of mitochondrial membrane potential in Jurkat T cells were shown to be inhibited by mitochondrial complex I inhibitor rotenone, suggesting that mitochondrial ROS might be important in radiation-induced caspase-dependent apoptosis. |
34(0,1,1,4) | Details |
| 19633536 | Li Y, Rory Goodwin C, Sang Y, Rosen EM, Laterra J, Xia S: Camptothecin and Fas receptor agonists synergistically induce medulloblastoma cell death: ROS-dependent mechanisms. Anticancer Drugs. 2009 Oct;20(9):770-8. Moreover, the mitochondrial respiratory chain complex I inhibitor rotenone potentiated CH-11-induced apoptosis in DAOY cells. Synergistic cell death was found to be predominantly apoptotic involving both extrinsic and intrinsic pathways as evidenced by annexin V staining, cleavage of caspases (3, 8, and 9), Bid and PARP, and cytoprotection by caspase inhibitors. |
1(0,0,0,1) | Details |
| 15192326 | Hail N Jr, Lotan R: Apoptosis induction by the natural product cancer chemopreventive agent deguelin is mediated through the inhibition of mitochondrial bioenergetics. Apoptosis. 2004 Jul;9(4):437-47. Furthermore, short-term exposure to deguelin diminished consumption by the parental cells and promoted mitochondrial permeability transition as evidenced by the dissipation of mitochondrial inner transmembrane potential, reactive species production, peroxidation, caspase activation, and mitochondrial swelling. |
1(0,0,0,1) | Details |
| 19224578 | Gill MB, Perez-Polo JR: Bax shuttling after rotenone treatment of neuronal primary cultures: effects on cell death phenotypes. J Neurosci Res. 2009 Jul;87(9):2047-65. The 25 microM rotenone treatment promptly increased nuclear Bax levels followed by a later increase in mitochondrial Bax levels and caspase-mediated cleavage of alpha-fodrin. |
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 |
| 18402771 | Lee J, Huang MS, Yang IC, Lai TC, Wang JL, Pang VF, Hsiao M, Kuo MY: Essential roles of caspases and their upstream regulators in rotenone-induced apoptosis. Biochem Biophys Res Commun. 2008 Jun 20;371(1):33-8. Epub 2008 Apr 8. |
18(0,0,3,3) | Details |
| 10549166 | Khar A, Ali AM, Begum Z, Pardhasaradhi BV, Varalakshmi C: Induction of apoptosis in AK-5 cells by rotenone involves participation of caspases. Indian J Biochem Biophys. 1999 Apr;36(2):77-81. |
6(0,0,1,1) | Details |
| 9804614 | Leist M, Volbracht C, Fava E, Nicotera P: 1-Methyl-4-phenylpyridinium induces autocrine excitotoxicity, protease activation, and neuronal apoptosis. Mol Pharmacol. 1998 Nov;54(5):789-801. The neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and other mitochondrial inhibitors (e.g., rotenone or 3-nitropropionic acid) elicited apoptosis in cerebellar granule cell cultures via stimulation of autocrine excitotoxicity. Two classes of proteases were involved in the execution of cell death: caspases and calpains. |
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 |
| 17102131 | Brown NM, Martin SM, Maurice N, Kuwana T, Knudson CM: Caspase inhibition blocks cell death and results in cell cycle arrest in cytokine-deprived hematopoietic cells. J Biol Chem. 2007 Jan 26;282(4):2144-55. Epub 2006 Nov 13. Furthermore, the "rescued" cells were resistant to rotenone, an inhibitor of mitochondrial respiration. |
1(0,0,0,1) | Details |
| 14743397 | Shih CM, Ko WC, Wu JS, Wei YH, Wang LF, Chang EE, Lo TY, Cheng HH, Chen CT: Mediating of caspase-independent apoptosis by cadmium through the mitochondria-ROS pathway in MRC-5 fibroblasts. J Cell Biochem. 2004 Feb 1;91(2):384-97. Using inhibitors of the mitochondrial electron transport chain (ETC) (oligomycin A and rotenone for complex I and V, respectively) and mitochondrial permeability transition pore (MPTP) (cyclosporin A and aristolochic acid), we coincidently found the ROS production, mitochondrial membrane depolarization, and apoptotic content were almost completely or partially abolished. |
6(0,0,0,6) | Details |
| 19111607 | Chen TY, Chi KH, Wang JS, Chien CL, Lin WW: Reactive species are involved in FasL-induced caspase-independent cell death and inflammatory responses. Free Radic Biol Med. 2009 Mar 1;46(5):643-55. Epub 2008 Dec 11. This death is associated with intracellular reactive species (ROS) production from mitochondria, as a ROS scavenger (BHA), antioxidants (trolox, NAC), and a mitochondrial respiratory chain uncoupler (rotenone) could prevent this event. |
5(0,0,0,5) | Details |
| 9349553 | Schulz JB, Bremen D, Reed JC, Lommatzsch J, Takayama S, Wullner U, Loschmann PA, Klockgether T, Weller M: Cooperative interception of neuronal apoptosis by BCL-2 and BAG-1 expression: prevention of caspase activation and reduced production of reactive species. J Neurochem. 1997 Nov;69(5):2075-86. |
5(0,0,0,5) | Details |
| 20018182 | Li J, Xu Z, Tan M, Su W, Gong XG: 3-(4-(Benzo [d] thiazol-2-yl)-1-phenyl-1H-pyrazol-3-yl) induced Hep G2 cell apoptosis through a ROS-mediated pathway. Chem Biol Interact. 2010 Feb 12;183(3):341-8. Epub 2009 Dec 16. DBP-5 caused massive ROS accumulation and GSH decrease, which lead to MMP disruption, caspase activation and finally induced cell apoptosis. Additionally, rotenone, an inhibitor of mitochondria electron transport system, effectively blocked the ROS elevated effect of DPB-5, which suggested that DPB-5-induced ROS generated from the mitochondria. |
1(0,0,0,1) | Details |
| 20042120 | Shaikh SB, Nicholson LF: Effects of chronic low dose rotenone treatment on human microglial cells. Mol Neurodegener. 2009 Dec 31;4:55. Levels of active caspases and ROS (both extra and intra cellular) were measured using biochemical methods. |
1(0,0,0,1) | Details |
| 11741286 | Armstrong JS, Hornung B, Lecane P, Jones DP, Knox SJ: Rotenone-induced G2/M cell cycle arrest and apoptosis in a human B lymphoma cell line PW. Biochem Biophys Res Commun. 2001 Dec 21;289(5):973-8. |
0(0,0,0,0) | Details |
| 16157303 | Nutku E, Hudson SA, Bochner BS: Mechanism of Siglec-8-induced human eosinophil apoptosis: role of caspases and mitochondrial injury. Biochem Biophys Res Commun. 2005 Oct 28;336(3):918-24. Rotenone and antimycin, inhibitors of mitochondrial respiratory chain components, completely inhibited apoptosis. |
4(0,0,0,4) | Details |
| 19631247 | Liang JH, Du J, Xu LD, Jiang T, Hao S, Bi J, Jiang B: Catalpol protects primary cultured cortical neurons induced by Abeta (1-42) through a mitochondrial-dependent caspase pathway. Neurochem Int. 2009 Dec;55(8):741-6. Epub 2009 Jul 22. It has been reported that catalpol, an iridoid glucoside, isolated from the root of Rehmannia glutinosa, protected cells from damage induced by a variety of toxic stimulus such as LPS, MPP (+) and rotenone. |
3(0,0,0,3) | Details |
| 15182854 | Lemarie A, Lagadic-Gossmann D, Morzadec C, Allain N, Fardel O, Vernhet L: Cadmium induces caspase-independent apoptosis in liver Hep3B cells: role for in signaling oxidative stress-related impairment of mitochondria and relocation of endonuclease G and apoptosis-inducing factor. Free Radic Biol Med. 2004 Jun 15;36(12):1517-31. Production of reactive species was inhibited by ruthenium red and rotenone, two mitochondrial inhibitors, and by diphenyleneiodonium, a flavoprotein inhibitor, which also prevented both loss in mitochondrial membrane potential and apoptosis. |
3(0,0,0,3) | Details |
| 12952965 | Grether-Beck S, Felsner I, Brenden H, Krutmann J: Mitochondrial cytochrome c release mediates -induced activator protein 2 activation and gene expression in keratinocytes. J Biol Chem. 2003 Nov 28;278(48):47498-507. Epub 2003 Sep 2. Inhibitors of mitochondrial electron transport chain (e.g. rotenone, thenoyltrifluoroacetone, and antimycin A) reduced -induced ICAM-1 expression. |
0(0,0,0,0) | Details |
| 12153473 | Poppe M, Reimertz C, Munstermann G, Kogel D, Prehn JH: -induced apoptosis of D283 medulloblastoma cells requires mitochondrial respiratory chain activity but occurs independently of caspases and is not sensitive to Bcl-xL overexpression. J Neurochem. 2002 Aug;82(3):482-94. Treatment with the complex I inhibitor rotenone, C2- or C8- induced cell death in D283 control cells, while rho- cells were significantly protected. |
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| 17035597 | Peng XH, Karna P, O'Regan RM, Liu X, Naithani R, Moriarty RM, Wood WC, Lee HY, Yang L: Down-regulation of inhibitor of apoptosis proteins by deguelin selectively induces apoptosis in breast cancer cells. Mol Pharmacol. 2007 Jan;71(1):101-11. Epub 2006 Oct 11. It is noteworthy that we detected an elevated level of cleaved poly (ADP- polymerase, a signature of caspase activation, without a significant increase in caspase activity in deguelin-treated cancer cells. |
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| 18485875 | Martinvalet D, Dykxhoorn DM, Ferrini R, Lieberman J: Granzyme A cleaves a mitochondrial complex I protein to initiate caspase-independent cell death. Cell. 2008 May 16;133(4):681-92. |
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| 16990509 | Moungjaroen J, Nimmannit U, Callery PS, Wang L, Azad N, Lipipun V, Chanvorachote P, Rojanasakul Y: Reactive species mediate caspase activation and apoptosis induced by in human lung epithelial cancer cells through Bcl-2 down-regulation. J Pharmacol Exp Ther. 2006 Dec;319(3):1062-9. Epub 2006 Sep 21. Likewise, the mitochondrial respiratory chain inhibitor rotenone potently inhibited the apoptotic and ROS-inducing effects of LA, supporting the role of mitochondrial ROS in LA-induced cell death. |
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| 17581813 | Marella M, Seo BB, Matsuno-Yagi A, Yagi T: Mechanism of cell death caused by complex I defects in a rat dopaminergic cell line. J Biol Chem. 2007 Aug 17;282(33):24146-56. Epub 2007 Jun 20. We have shown that expression of a rotenone-insensitive yeast -quinone oxidoreductase (Ndi1) can rescue mammalian cells from complex I dysfunction. |
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| 12821677 | Ling YH, Liebes L, Zou Y, Perez-Soler R: Reactive species generation and mitochondrial dysfunction in the apoptotic response to Bortezomib, a novel proteasome inhibitor, in human H460 non-small cell lung cancer cells. J Biol Chem. 2003 Sep 5;278(36):33714-23. Epub 2003 Jun 23. Co-incubation with rotenone and antimycin A, inhibitors of mitochondrial electron transport chain complexes I and III, or with cyclosporine A, an inhibitor of mitochondrial permeability transition pore, resulted in inhibition of bortezomib-induced ROS generation, increase in Delta psi m, and cytochrome c release. |
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| 10366439 | Leist M, Single B, Naumann H, Fava E, Simon B, Kuhnle S, Nicotera P: Inhibition of mitochondrial ATP generation by switches apoptosis to necrosis. Exp Cell Res. 1999 Jun 15;249(2):396-403. In contrast, depleting intracellular ATP with rotenone, an inhibitor of mitochondrial complex I mimicked the effect of NO. In the presence of NO, release of mitochondrial cytochrome c was delayed and activation of execution caspases was prevented. |
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| 15808420 | Aronis A, Madar Z, Tirosh O: Mechanism underlying oxidative stress-mediated lipotoxicity: exposure of J774.2 macrophages to triacylglycerols facilitates mitochondrial reactive species production and cellular necrosis. Free Radic Biol Med. 2005 May 1;38(9):1221-30. TG-mediated ROS production was demonstrated to be via mitochondrial complex 1 of the electron-transfer chain since the inhibitor of complex 1 rotenone significantly attenuated the cellular ROS levels in TG-treated cells. We therefore evaluated the effect of TG on apoptotic cells showing high caspase activity. |
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| 14732287 | Herrera B, Murillo MM, Alvarez-Barrientos A, Beltran J, Fernandez M, Fabregat I: Source of early reactive species in the apoptosis induced by transforming growth factor-beta in fetal rat hepatocytes. Free Radic Biol Med. 2004 Jan 1;36(1):16-26. Rotenone, an inhibitor of the NADH dehydrogenase in mitochondrial complex I, attenuated, but did not completely inhibit, ROS-production, caspase activation, and cell death mediated by TGF-beta. |
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| 15812315 | King TD, Jope RS: Inhibition of glycogen synthase kinase-3 protects cells from intrinsic but not extrinsic oxidative stress. Neuroreport. 2005 Apr 25;16(6):597-601. Both intrinsic oxidative stress induced by the mitochondrial inhibitor rotenone and extrinsic oxidative stress induced by exogenously added H2O2 activated Bax, caspase-2, and caspase-3 in human neuroblastoma SH-SY5Y cells. |
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