| Name | alpha synuclein |
|---|---|
| Synonyms | Alpha synuclein; PARK4; PD1; NACP; Non A beta component of AD amyloid; Non A4 component of amyloid; Non A4 component of amyloid precursor; PARK 1… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17690729 | Feng Y, Liang ZH, Wang T, Qiao X, Liu HJ, Sun SG: alpha-Synuclein redistributed and aggregated in rotenone-induced Parkinson's disease rats. Neurosci Bull. 2006 Sep;22(5):288-93. |
13(0,0,2,3) | Details |
| 15099020 | Dalfo E, Gomez-Isla T, Rosa JL, Nieto Bodelon M, Cuadrado Tejedor M, Barrachina M, Ambrosio S, Ferrer I: Abnormal alpha-synuclein interactions with Rab proteins in alpha-synuclein A30P transgenic mice. J Neuropathol Exp Neurol. 2004 Apr;63(4):302-13. Aggregates of alpha-synuclein, although with different molecular weights, were also observed in rotenone-treated Tg and wildtype mice. |
13(0,0,1,8) | Details |
| 18335520 | Shaikh S, Nicholson LF: Advanced glycation end products induce in vitro cross-linking of alpha-synuclein and accelerate the process of intracellular inclusion body formation. J Neurosci Res. 2008 Jul;86(9):2071-82. We first investigated the time-dependent cross-linking of recombinant human alpha-synuclein in the presence of AGEs in vitro, then used a cell culture model based on chronic rotenone treatment of human dopaminergic neuroblastoma cells (SH-SY5Y) over a period of 1-4 weeks, in the presence of different doses of AGEs. |
11(0,0,1,6) | Details |
| 11535288 | Shastry BS: Parkinson disease: etiology, pathogenesis and future of gene therapy. Neurosci Res. 2001 Sep;41(1):5-12. Two of these genes are involved in the ubiquitin mediated pathway of protein degradation and the third one is a highly expressed protein in the synaptic terminal and is called alpha-synuclein. In animal models, it has been shown that use of the household pesticide which is known to contain rotenone, causes PD. |
1(0,0,0,1) | Details |
| 15462376 | Ogawa N, Asanuma M, Miyoshi K: [Mechanism of specific dopaminergic neuronal death in Parkinson's disease] . Nippon Rinsho. 2004 Sep;62(9):1629-34. The free radicals/oxidative stress produced by MPTP, rotenone, activated microglias, and disturbances in mitochondrial respiratory enzymes provide a common pathway for the progression of all kinds of neurons. For example, the formation of DA -alpha-synuclein complex consequently increases cytotoxic protofibrils and covalent modification of functional enzymes. |
1(0,0,0,1) | Details |
| 11948617 | Betarbet R, Sherer TB, Greenamyre JT: Animal models of Parkinson's disease. Bioessays. 2002 Apr;24(4):308-18. Recently, it has been found that agricultural chemicals, such as rotenone and paraquat, when administered systemically, can reproduce specific features of PD in rodents, apparently via oxidative damage. Transgenic animals that over-express alpha-synuclein are used to study the role of this protein in dopaminergic degeneration. |
1(0,0,0,1) | Details |
| 17131421 | Fountaine TM, Wade-Martins R: RNA interference-mediated knockdown of alpha-synuclein protects human dopaminergic neuroblastoma cells from MPP (+) toxicity and reduces transport. J Neurosci Res. 2007 Feb 1;85(2):351-63. We show that alpha-synuclein knockdown has no effect on cellular survival either under normal growth conditions over 5 days or in the presence of the mitochondrial inhibitor rotenone. |
10(0,0,0,10) | Details |
| 11445065 | Uversky VN, Li J, Fink AL: Pesticides directly accelerate the rate of alpha-synuclein fibril formation: a possible factor in Parkinson's disease. FEBS Lett. 2001 Jul 6;500(3):105-8. Here we show that several pesticides, including rotenone, dieldrin and paraquat, induce a conformational change in alpha-synuclein and significantly accelerate the rate of formation of alpha-synuclein fibrils in vitro. |
9(0,0,1,4) | Details |
| 15530876 | Ling Z, Chang QA, Tong CW, Leurgans SE, Lipton JW, Carvey PM: Rotenone potentiates neuron loss in animals exposed to lipopolysaccharide prenatally. Exp Neurol. 2004 Dec;190(2):373-83. Prenatal LPS exposure also led to increased levels of oxidized proteins and the formation of alpha-Synuclein and eosin positive inclusions resembling Lewy bodies. |
1(0,0,0,1) | Details |
| 20030238 | Takahashi R, Kawamata J, Takeuchi H: [Pathogenesis of sporadic Parkinson's disease: contribution of genetic and environmental risk factors]. Rinsho Shinkeigaku. 2009 Nov;49(11):885-7. Alpha synuclein (a-SYN) and the disturbance of a-SYN metabolism seems to play the most important role in PD pathogenesis. a-SYN, the gene causative in PARK1, is the major component of Lewy bodies. Mitochondrial complex I inhibitors, such as MPTP and rotenone, induce selective dopaminergic neuronal death, suggesting that chemicals may constitute risk factors of sporadic PD. |
1(0,0,0,1) | Details |
| 19198139 | Takeda A, Sugeno N, Hasegawa T, Kobayashi M, Kikuchi A: [Cellular pathophysiology of Parkinson's disease] . Rinsho Shinkeigaku. 2008 Nov;48(11):984-5. The data thus obtained suggested the followings. (1) By the treatment with rotenone, wild type alpha-synuclein overexpressing cells demonstrated intracellular aggregations, which shared a number of features with Lewy bodies. (2) The aggregate formation of alpha-synuclein may be cytoprotective. (3) The -derived quinones are candidate molecules to facilitate the oligomer formation of a-synuclein. (4) The cells overexpressing S129A mutant showed few aggregations. |
8(0,0,1,3) | Details |
| 18155613 | Ravenstijn PG, Merlini M, Hameetman M, Murray TK, Ward MA, Lewis H, Ball G, Mottart C, de Ville de Goyet C, Lemarchand T, van Belle K, O'Neill MJ, Danhof M, de Lange EC: The exploration of rotenone as a toxin for inducing Parkinson's disease in rats, for application in BBB transport and PK-PD experiments. J Pharmacol Toxicol Methods. 2008 Mar-Apr;57(2):114-30. Epub 2007 Nov 13. At different times following rotenone infusion, behaviour, histopathology (tyrosine hydroxylase and alpha-synuclein immunocytochemistry), peripheral organ pathology (adrenals, heart, kidney, liver, lung, spleen and stomach) were assessed. |
7(0,0,1,2) | Details |
| 19850127 | Ruan Q, Harrington AJ, Caldwell KA, Caldwell GA, Standaert DG: VPS41, a protein involved in lysosomal trafficking, is protective in Caenorhabditis elegans and mammalian cellular models of Parkinson's disease. Neurobiol Dis. 2010 Feb;37(2):330-8. Epub 2009 Oct 20. VPS41 has a plausible mechanistic link to the pathogenesis of PD, as in yeast it is known to participate in trafficking of proteins to the lysosomal system and several recent lines of evidence have pointed to the importance of lysosomal system dysfunction in the neurotoxicity of alpha-synuclein (alpha-syn). In SH-SY5Y neuroblastoma cell lines stably transfected with hVPS41, we determined that presence of this protein conferred protection against the neurotoxins 6-OHDA and rotenone. |
1(0,0,0,1) | Details |
| 20098733 | Pan-Montojo F, Anichtchik O, Dening Y, Knels L, Pursche S, Jung R, Jackson S, Gille G, Spillantini MG, Reichmann H, Funk RH: Progression of Parkinson's disease pathology is reproduced by intragastric administration of rotenone in mice. PLoS One. 2010 Jan 19;5(1):e8762. Our results show that low doses of chronically and intragastrically administered rotenone induce alpha-synuclein accumulation in all the above-mentioned nervous system structures of wild-type mice. |
6(0,0,1,1) | Details |
| 15790535 | Testa CM, Sherer TB, Greenamyre JT: Rotenone induces oxidative stress and dopaminergic neuron damage in organotypic substantia nigra cultures. Brain Res Mol Brain Res. 2005 Mar 24;134(1):109-18. Epub 2005 Jan 6. Greenamyre, Subcutaneous rotenone exposure causes highly selective dopaminergic degeneration and alpha-synuclein aggregation, Exp. |
6(0,0,1,1) | Details |
| 17459145 | Inden M, Kitamura Y, Takeuchi H, Yanagida T, Takata K, Kobayashi Y, Taniguchi T, Yoshimoto K, Kaneko M, Okuma Y, Taira T, Ariga H, Shimohama S: Neurodegeneration of mouse nigrostriatal dopaminergic system induced by repeated oral administration of rotenone is prevented by a chemical chaperone. J Neurochem. 2007 Jun;101(6):1491-1504. Chronic oral administration of rotenone at high doses induced specific nigrostriatal DA neurodegeneration, motor deficits and the up-regulation of alpha-synuclein in the surviving DA neurons. |
6(0,0,1,1) | Details |
| 14985429 | Lee HJ, Khoshaghideh F, Patel S, Lee SJ: Clearance of alpha-synuclein oligomeric intermediates via the lysosomal degradation pathway. J Neurosci. 2004 Feb 25;24(8):1888-96. |
6(0,0,0,6) | Details |
| 12941575 | Di Monte DA: The environment and Parkinson's disease: is the nigrostriatal system preferentially targeted by neurotoxins?. Lancet Neurol. 2003 Sep;2(9):531-8. New models of selective nigrostriatal damage--such as neurotoxicity induced by rotenone or paraquat--have emphasised that environmental agents may contribute to the neurodegenerative process in PD. Toxins interact, in vitro and in vivo, with alpha-synuclein, an endogenous protein that is implicated in pathology of PD. |
1(0,0,0,1) | Details |
| 18624765 | Zhang H, Jia H, Liu J, Ao N, Yan B, Shen W, Wang X, Li X, Luo C, Liu J: Combined R- and exerts efficient preventative effects in a cellular model of Parkinson's disease. J Cell Mol Med. 2008 Jun 20. We demonstrated that 4-week pretreatment with LA and/or ALC effectively protected SK-N-MC human neuroblastoma cells against rotenone-induced mitochondrial dysfunction, oxidative damage, and accumulation of alpha-synuclein and ubiquitin. |
6(0,0,1,1) | Details |
| 20038714 | Su LJ, Auluck PK, Outeiro TF, Yeger-Lotem E, Kritzer JA, Tardiff DF, Strathearn KE, Liu F, Cao S, Hamamichi S, Hill KJ, Caldwell KA, Bell GW, Fraenkel E, Cooper AA, Caldwell GA, McCaffery JM, Rochet JC, Lindquist S: Compounds from an unbiased chemical screen reverse both ER-to-Golgi trafficking defects and mitochondrial dysfunction in Parkinson's disease models. Dis Model Mech. 2010 Mar-Apr;3(3-4):194-208. Epub 2009 Dec 28. Remarkably, the compounds also protected neurons against rotenone-induced toxicity, which has been used to model the mitochondrial defects associated with PD in humans. alpha-Synuclein (alpha-syn) is a small lipid-binding protein involved in vesicle trafficking whose function is poorly characterized. |
1(0,0,0,1) | Details |
| 19409963 | Caudle WM, Kitsou E, Li J, Bradner J, Zhang J: A role for a novel protein, nucleolin, in Parkinson's disease. Neurosci Lett. 2009 Jul 31;459(1):11-5. Epub 2009 May 4. Previously, in a cellular model of PD, we identified nucleolin as a protein interacting with alpha-synuclein and DJ-1, two critical proteins involved in PD pathogenesis. Furthermore, manipulation of nucleolin in an in vitro model of PD resulted in significant alterations in the generation of oxidative stress as well as proteasomal inhibition following rotenone exposure. |
1(0,0,0,1) | Details |
| 18562315 | Sugeno N, Takeda A, Hasegawa T, Kobayashi M, Kikuchi A, Mori F, Wakabayashi K, Itoyama Y: Serine 129 phosphorylation of alpha-synuclein induces unfolded protein response-mediated cell death. J Biol Chem. 2008 Aug 22;283(34):23179-88. Epub 2008 Jun 18. Following the treatment with rotenone, a mitochondrial complex I inhibitor, wild type alpha-synuclein-overexpressing cells demonstrated intracellular aggregations, which shared a number of features with Lewy bodies, although cells overexpressing the S129A mutant, in which phosphorylation at Ser (129) was blocked, showed few aggregations. |
168(2,2,2,8) | Details |
| 12548372 | Vanacore N, Nappo A, Gentile M, Brustolin A, Palange S, Liberati A, Di Rezze S, Caldora G, Gasparini M, Benedetti F, Bonifati V, Forastiere F, Quercia A, Meco G: Evaluation of risk of Parkinson's disease in a cohort of licensed pesticide users. Neurol Sci. 2002 Sep;23 Suppl 2:S119-20. From an experimental point of view, a new model of parkinsonism induced by rotenone, a diffuse insecticide, has been proposed, and in vitro studies have provided proof that several pesticides stimulate the formation of alpha-synuclein fibrils (one of the principal constituents of Lewy bodies). |
6(0,0,1,1) | Details |
| 15084427 | Alam M, Mayerhofer A, Schmidt WJ: The neurobehavioral changes induced by bilateral rotenone lesion in medial forebrain bundle of rats are reversed by Behav Brain Res. 2004 May 5;151(1-2):117-24. Rotenone (an inhibitor of mitochondrial complex I) has been proposed as a model of Parkinson's disease (PD) as it induces nigrostriatal degeneration associated with alpha-synuclein inclusions. |
1(0,0,0,1) | Details |
| 15265640 | Alam M, Schmidt WJ: reverses the hypokinetic behaviour and rigidity in rotenone-treated rats. Behav Brain Res. 2004 Aug 31;153(2):439-46. Peripherally and locally administered rotenone (an inhibitor of mitochondrial complex I) has been proposed as a model of Parkinson's disease (PD) as it induces nigrostriatal degeneration associated with alpha-synuclein inclusions. |
1(0,0,0,1) | Details |
| 15893636 | Diaz-Corrales FJ, Asanuma M, Miyazaki I, Miyoshi K, Ogawa N: Rotenone induces aggregation of gamma-tubulin protein and subsequent disorganization of the centrosome: relevance to formation of inclusion bodies and neurodegeneration. Neuroscience. 2005;133(1):117-35. These centrosomes also displayed multiple aggregates of alpha-synuclein protein. |
1(0,0,0,1) | Details |
| 15280438 | Watabe M, Nakaki T: Rotenone induces apoptosis via activation of bad in human dopaminergic SH-SY5Y cells. J Pharmacol Exp Ther. 2004 Dec;311(3):948-53. Epub 2004 Jul 27. Because Bad and alpha-synuclein are known to bind to 14-3-3 proteins, we examined the effects of rotenone on these complexes. |
149(1,3,4,4) | 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. Chronic systemic complex I inhibition caused by rotenone exposure induces features of Parkinson's disease (PD) in rats, including selective nigrostriatal dopaminergic degeneration and formation of ubiquitin- and alpha-synuclein-positive inclusions (Betarbet et al., 2000). |
100(0,3,4,5) | Details |
| 11100151 | Betarbet R, Sherer TB, MacKenzie G, Garcia-Osuna M, Panov AV, Greenamyre JT: Chronic systemic pesticide exposure reproduces features of Parkinson's disease. Nat Neurosci. 2000 Dec;3(12):1301-6. Nigral neurons in rotenone-treated rats accumulate fibrillar cytoplasmic inclusions that contain ubiquitin and alpha-synuclein. |
6(0,0,1,1) | Details |
| 16774923 | Ogburn KD, Figueiredo-Pereira ME: Cytoskeleton/endoplasmic reticulum collapse induced by parallels centrosomal deposition of ubiquitinated protein aggregates. J Biol Chem. 2006 Aug 11;281(32):23274-84. Epub 2006 Jun 14. This aberrant protein deposition, triggered by a product of inflammation, may be common to other compounds that disrupt microtubules and induce protein aggregation, such as MPP+ and rotenone, found to be associated with neurodegeneration. This cyclopentenone prostaglandin triggered endoplasmic reticulum (ER) collapse and the redistribution of ER proteins, such as calnexin and catechol-O-methyltransferase, into a large centrosomal aggregate containing ubiquitinated proteins and alpha-synuclein. |
1(0,0,0,1) | Details |
| 19114014 | Borland MK, Trimmer PA, Rubinstein JD, Keeney PM, Mohanakumar K, Liu L, Bennett JP Jr: Chronic, low-dose rotenone reproduces Lewy neurites found in early stages of Parkinson's disease, reduces mitochondrial movement and slowly kills differentiated SH-SY5Y neural cells. Mol Neurodegener. 2008 Dec 29;3:21. ABSTRACT: BACKGROUND: Parkinson's disease, the most common adult neurodegenerative movement disorder, demonstrates a brain-wide pathology that begins pre-clinically with alpha-synuclein aggregates ("Lewy neurites") in processes of gut enteric and vagal motor neurons. |
1(0,0,0,1) | Details |
| 17017540 | Hoglinger GU, Oertel WH, Hirsch EC: The rotenone model of parkinsonism--the five years inspection. J Neural Transm Suppl. 2006;(70):269-72. |
0(0,0,0,0) | Details |
| 16439141 | Betarbet R, Canet-Aviles RM, Sherer TB, Mastroberardino PG, McLendon C, Kim JH, Lund S, Na HM, Taylor G, Bence NF, Kopito R, Seo BB, Yagi T, Yagi A, Klinefelter G, Cookson MR, Greenamyre JT: Intersecting pathways to neurodegeneration in Parkinson's disease: effects of the pesticide rotenone on DJ-1, alpha-synuclein, and the ubiquitin-proteasome system. Neurobiol Dis. 2006 May;22(2):404-20. Epub 2006 Jan 24. Chronic rotenone exposure in vivo caused oxidative modification of DJ-1, accumulation of alpha-synuclein, and proteasomal impairment. |
90(1,1,2,5) | Details |
| 14550906 | Orth M, Tabrizi SJ, Schapira AH, Cooper JM: Alpha-synuclein expression in HEK293 cells enhances the mitochondrial sensitivity to rotenone. Neurosci Lett. 2003 Nov 6;351(1):29-32. However, both wild-type and mutant G209A alpha-synuclein expression enhanced the fall in mitochondrial membrane potential induced by the complex I inhibitor rotenone. |
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| 19681169 | Tapias V, Cannon JR, Greenamyre JT: treatment potentiates neurodegeneration in a rat rotenone Parkinson's disease model. J Neurosci Res. 2010 Feb 1;88(2):420-7. The rat rotenone model reproduces many of the pathological features of the human disease, including apomorphine-responsive behavioral deficits, DA depletion, loss of striatal DA terminals and nigral dopaminergic neurons, and alpha-synuclein/polyubiquitin-positive cytoplasmic inclusions reminiscent of Lewy bodies. |
6(0,0,1,1) | Details |
| 19385059 | Cannon JR, Tapias V, Na HM, Honick AS, Drolet RE, Greenamyre JT: A highly reproducible rotenone model of Parkinson's disease. Neurobiol Dis. 2009 May;34(2):279-90. Additionally, in rotenone-treated animals, alpha-synuclein and poly-ubiquitin positive aggregates were observed in neurons of the substantia nigra. |
6(0,0,1,1) | Details |
| 19860724 | Agnati FL, Guidolin D, Baluska F, Leo G, Barlow PW, Carone C, Genedani S: A New Hypothesis of Pathogenesis Based on the Divorce between Mitochondria and their Host Cells: Possible Relevances for the Alzheimer's Disease. Curr Alzheimer Res. 2009 Sep 28. Furthermore, the present data demonstrate the presence of alpha-synuclein (alpha-syn) within TNTs, hence a similar pathogenic mechanism to the one surmised for AD, but centred on alpha-syn rather than on Abeta, may play a role in Parkinson's Disease (PD). This proposal finds indirect support from observations on rotenone-poisoned glioblastoma cells which have been co-cultured with non-poisoned cells. |
1(0,0,0,1) | Details |
| 19647776 | Inden M, Kitamura Y, Tamaki A, Yanagida T, Shibaike T, Yamamoto A, Takata K, Yasui H, Taira T, Ariga H, Taniguchi T: Neuroprotective effect of the antiparkinsonian drug pramipexole against nigrostriatal dopaminergic degeneration in rotenone-treated mice. Neurochem Int. 2009 Dec;55(8):760-7. Epub 2009 Aug 6. Pramipexole inhibited rotenone-induced DA neuronal death and motor deficits, and reduced immunoreactivity for alpha-synuclein. |
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| 19595768 | Drolet RE, Cannon JR, Montero L, Greenamyre JT: Chronic rotenone exposure reproduces Parkinson's disease gastrointestinal neuropathology. Neurobiol Dis. 2009 Oct;36(1):96-102. Epub 2009 Jul 10. Rotenone treatment caused an acute reduction in alpha-synuclein-immunoreactivity, but this was followed 6 months later by a robust increase in aggregate pathology and cytoplasmic inclusions that were similar in appearance to enteric Lewy-bodies in idiopathic PD. |
88(1,1,2,3) | Details |
| 17273802 | Luo C, Rajput AH, Akhtar S, Rajput A: Alpha-synuclein and tyrosine hydroxylase expression in acute rotenone toxicity. Int J Mol Med. 2007 Mar;19(3):517-21. In the substantia nigra of rotenone-treated rats, four of six had reduced numbers of tyrosine hydroxylase-positive neurons and all six had increased nigral alpha-synuclein expression. |
87(1,1,2,2) | Details |
| 16584840 | Lev N, Melamed E, Offen D: Proteasomal inhibition hypersensitizes differentiated neuroblastoma cells to oxidative damage. Neurosci Lett. 2006 May 15;399(1-2):27-32. Epub 2006 Apr 11. Alpha-synuclein is of particular interest in PD since it is a major component of Lewy bodies and mutations in the alpha-synuclein gene were identified in familial PD. Naive and transfected cells were exposed to oxidative stress induced by rotenone, SIN-I, FeCl (2,) and to proteasomal inhibition by lactacystin. |
5(0,0,0,5) | Details |
| 11724769 | Lee HJ, Shin SY, Choi C, Lee YH, Lee SJ: Formation and removal of alpha-synuclein aggregates in cells exposed to mitochondrial inhibitors. J Biol Chem. 2002 Feb 15;277(7):5411-7. Epub 2001 Nov 27. Treatment with rotenone, an inhibitor of complex I, resulted in an increase of detergent-resistant alpha-synuclein aggregates and a reduction in ATP level. |
5(0,0,0,5) | Details |
| 19628769 | Yu WH, Dorado B, Figueroa HY, Wang L, Planel E, Cookson MR, Clark LN, Duff KE: Metabolic activity determines efficacy of macroautophagic clearance of pathological oligomeric alpha-synuclein. Am J Pathol. 2009 Aug;175(2):736-47. Epub 2009 Jul 23. Finally, rotenone-induced alpha-syn aggregates were cleared following rapamycin stimulation of autophagy. |
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| 15026413 | Hashimoto M, Bar-On P, Ho G, Takenouchi T, Rockenstein E, Crews L, Masliah E: Beta-synuclein regulates Akt activity in neuronal cells. J Biol Chem. 2004 May 28;279(22):23622-9. Epub 2004 Mar 16. Recent studies have shown that the neurodegenerative process in disorders with Lewy body formation, such as Parkinson's disease and dementia with Lewy bodies, is associated with alpha-synuclein accumulation and that beta-synuclein might protect the central nervous system from the effects of alpha-synuclein. Beta-synuclein transfection resulted in increased Akt activity and conferred protection from the effects of rotenone. |
2(0,0,0,2) | Details |
| 12807439 | Jensen PJ, Alter BJ, O'Malley KL: Alpha-synuclein protects naive but not dbcAMP-treated dopaminergic cell types from 1-methyl-4-phenylpyridinium toxicity. J Neurochem. 2003 Jul;86(1):196-209. Similarly, alpha-synuclein protected cells from the complex I inhibitor rotenone and 3-nitroproprionic acid, a complex II inhibitor. |
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| 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. |
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| 18331584 | Liu F, Nguyen JL, Hulleman JD, Li L, Rochet JC: Mechanisms of DJ-1 neuroprotection in a cellular model of Parkinson's disease. J Neurochem. 2008 Apr 15. Mitochondrial dysfunction, proteasome inhibition, and alpha-synuclein aggregation are thought to play important roles in the pathogenesis of Parkinson's disease (PD). Expression of wild-type DJ-1 rescued primary dopaminergic neurons from toxicity elicited by rotenone, proteasome inhibitors, and mutant alpha-synuclein. |
3(0,0,0,3) | Details |
| 18514418 | Shavali S, Brown-Borg HM, Ebadi M, Porter J: Mitochondrial localization of alpha-synuclein protein in alpha-synuclein overexpressing cells. Neurosci Lett. 2008 Jul 11;439(2):125-8. Epub 2008 May 8. The goals of the present study were to examine whether alpha-syn is localized in the mitochondria of alpha-syn overexpressing cells (HEK-syn cells); and whether alpha-syn overexpression causes cells to be more vulnerable to mitochondrial toxin, rotenone. |
3(0,0,0,3) | Details |
| 19924288 | Xiong N, Huang J, Zhang Z, Zhang Z, Xiong J, Liu X, Jia M, Wang F, Chen C, Cao X, Liang Z, Sun S, Lin Z, Wang T: Stereotaxical infusion of rotenone: a reliable rodent model for Parkinson's disease. PLoS One. 2009 Nov 18;4(11):e7878. The rotenone infusion also reduced the DA content, the and superoxide dismutase activities, and induced alpha-synuclein expression, when compared to the contralateral side. |
81(1,1,1,1) | Details |
| 20117172 | Dadakhujaev S, Noh HS, Jung EJ, Cha JY, Baek SM, Ha JH, Kim DR: Autophagy protects the rotenone-induced cell death in alpha-synuclein overexpressing SH-SY5Y cells. Neurosci Lett. 2010 Mar 12;472(1):47-52. Epub 2010 Feb 1. Autophagy activation also restored the mitochondrial membrane potential (MMP) impaired by rotenone in mutant alpha-synuclein expressing cells. |
71(0,2,3,6) | Details |
| 17686240 | Wang L, Cao XB, Wang JM, Qu RS, Xu L, Qiao X, Sun SG: [Proteolytic stress induced by environmental toxins in dopaminergic neurons: an experimental study]. Zhonghua Yi Xue Za Zhi. 2007 May 8;87(17):1190-4. METHODS: Nerve growth factor-treated-rat adrenal pheochromocytoma cells of the line PC12 were co-incubated with (6-OHDA), 1-methyl-4-phenylpyridinium ion (MPP (+)), and rotenone for 24 hours. The expression levels of alpha-synuclein and ubiquited proteins in every group were observed with laser scanning confocal technique. |
3(0,0,0,3) | Details |
| 12880480 | Sharma SK, Ebadi M: Metallothionein attenuates 3-morpholinosydnonimine (SIN-1)-induced oxidative stress in dopaminergic neurons. Antioxid Redox Signal. 2003 Jun;5(3):251-64. The synthesis of mitochondrial and apoptosis-inducing factors were increased following exposure to 1-methyl-4-phenylpyridinium ion or rotenone. In addition, it caused DNA fragmentation, alpha-synuclein induction, and intramitochondrial accumulation of metal ions iron, zinc, and and enhanced the synthesis of |
3(0,0,0,3) | Details |
| 16854843 | Jin J, Li GJ, Davis J, Zhu D, Wang Y, Pan C, Zhang J: Identification of novel proteins associated with both alpha-synuclein and DJ-1. Mol Cell Proteomics. 2007 May;6(5):845-59. Epub 2006 Jul 18. Of those, 114 proteins displayed significant changes in the relative abundance in the complexes associated with alpha-synuclein, DJ-1, or both after rotenone treatment. |
49(0,1,3,9) | Details |
| 11679584 | Lee HJ, Choi C, Lee SJ: Membrane-bound alpha-synuclein has a high aggregation propensity and the ability to seed the aggregation of the cytosolic form. J Biol Chem. 2002 Jan 4;277(1):671-8. Epub 2001 Oct 25. In our recent study, we showed that mitochondrial inhibitors such as rotenone, induced alpha-synuclein aggregation in cells. |
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| 18289173 | Lin CH, Huang JY, Ching CH, Chuang JI: reduces the neuronal loss, downregulation of dopamine transporter, and upregulation of D2 receptor in rotenone-induced parkinsonian rats. J Pineal Res. 2008 Mar;44(2):205-13. Rotenone subcutaneously infused for 14 days induced PD symptoms in rats, as indicated by reduced spontaneous locomotor activity (hypokinesis), loss of tyrosine hydroxylase (TH, a marker enzyme for neurons) immunoreactivity in the substantia nigra and striatum, obvious alpha-synuclein accumulation, downregulated DAT protein expression, and upregulated D2R expression. |
37(0,1,2,2) | Details |
| 16579629 | Mirzaei H, Schieler JL, Rochet JC, Regnier F: Identification of rotenone-induced modifications in alpha-synuclein using affinity pull-down and tandem mass spectrometry. Anal Chem. 2006 Apr 1;78(7):2422-31. |
37(0,1,1,7) | Details |
| 18456002 | Liu F, Hindupur J, Nguyen JL, Ruf KJ, Zhu J, Schieler JL, Bonham CC, Wood KV, Davisson VJ, Rochet JC: Methionine sulfoxide reductase A protects dopaminergic cells from Parkinson's disease-related insults. Free Radic Biol Med. 2008 Aug 1;45(3):242-55. Epub 2008 Apr 11. PD pathogenesis involves mitochondrial dysfunction, proteasome impairment, and alpha-synuclein aggregation, insults that may be especially toxic to oxidatively stressed cells including dopaminergic neurons. Here, we show that MsrA suppresses dopaminergic cell death and protein aggregation induced by the complex I inhibitor rotenone or mutant alpha-synuclein, but not by the proteasome inhibitor MG132. |
2(0,0,0,2) | Details |
| 14535945 | Martin FL, Williamson SJ, Paleologou KE, Hewitt R, El-Agnaf OM, Allsop D: Fe (II)-induced DNA damage in alpha-synuclein-transfected human dopaminergic BE (2)-M17 neuroblastoma cells: detection by the Comet assay. J Neurochem. 2003 Nov;87(3):620-30. Susceptibility to Fe (II)-induced DNA damage appeared to be dependent on alpha-syn status because cells transfected with wild-type alpha-syn or A53T alpha-syn were equally susceptible to the damaging effects of the mitochondrial respiratory chain inhibitor rotenone. |
2(0,0,0,2) | Details |
| 16219024 | Hoglinger GU, Lannuzel A, Khondiker ME, Michel PP, Duyckaerts C, Feger J, Champy P, Prigent A, Medja F, Lombes A, Oertel WH, Ruberg M, Hirsch EC: The mitochondrial complex I inhibitor rotenone triggers a cerebral tauopathy. J Neurochem. 2005 Nov;95(4):930-9. Epub 2005 Aug 10. To determine experimentally whether chronic generalized complex I inhibition has an effect on the distribution of alpha-synuclein or tau, we infused rats systemically with the plant-derived isoflavonoid rotenone. |
34(0,1,1,4) | Details |
| 16006012 | Nieto M, Gil-Bea FJ, Dalfo E, Cuadrado M, Cabodevilla F, Sanchez B, Catena S, Sesma T, Ribe E, Ferrer I, Ramirez MJ, Gomez-Isla T: Increased sensitivity to MPTP in human alpha-synuclein A30P transgenic mice. Neurobiol Aging. 2006 Jun;27(6):848-56. Epub 2005 Jul 11. We investigated the possible interaction between genetic factors and neurotoxins by testing whether alpha-synuclein A30P Tg5093 transgenic mice show increased sensitivity to secondary toxic insults like 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or rotenone. |
33(0,1,1,3) | Details |
| 18715146 | Ethell DW, Fei Q: Parkinson-linked genes and toxins that affect neuronal cell death through the Bcl-2 family. Antioxid Redox Signal. 2009 Mar;11(3):529-40. Potential causative factors include environmental toxins and gene mutations that can combine to dysregulate the processing and degradation of alpha-synuclein. Oxidative stress induced by the neurotoxins MPTP, paraquat, maneb, and rotenone causes lipid peroxidation and protein misfolding that affects cell death through members of the Bcl-2 family. |
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| 17967736 | Paris I, Cardenas S, Lozano J, Perez-Pastene C, Graumann R, Riveros A, Caviedes P, Segura-Aguilar J: Aminochrome as a preclinical experimental model to study degeneration of dopaminergic neurons in Parkinson's disease. Neurotox Res. 2007 Sep;12(2):125-34. Different model neurotoxins have been used as preclinical experimental models to study the neurodegenerative process in PD, such as (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and rotenone. However, aminochrome itself can induce neurotoxicity under certain aberrant conditions such as (i) one-electron reduction of aminochrome catalyzed by flavoenzymes to leukoaminochrome o-semiquinone radical, which is a highly reactive neurotoxin; or (ii) the formation of aminochrome adducts with alpha-synuclein, enhancing and stabilizing the formation of protofibrils. |
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| 15234983 | Zhou Y, Gu G, Goodlett DR, Zhang T, Pan C, Montine TJ, Montine KS, Aebersold RH, Zhang J: Analysis of alpha-synuclein-associated proteins by quantitative proteomics. J Biol Chem. 2004 Sep 10;279(37):39155-64. Epub 2004 Jul 1. To identify the proteins associated with soluble alpha-synuclein (AS) that might promote AS aggregation, a key event leading to neurodegeneration, we quantitatively compared protein profiles of AS-associated protein complexes in MES cells exposed to rotenone, a pesticide that produces parkinsonism in animals and induces Lewy body (LB)-like inclusions in the remaining dopaminergic neurons, and to vehicle. |
32(0,1,1,2) | Details |
| 18639366 | Jia H, Liu Z, Li X, Feng Z, Hao J, Li X, Shen W, Zhang H, Liu J: Synergistic anti-Parkinsonism activity of high doses of B vitamins in a chronic cellular model. Neurobiol Aging. 2010 Apr;31(4):636-46. Epub 2008 Jul 17. Pretreatment with B vitamins (also 4 weeks) prevented rotenone-induced: (1) mitochondrial dysfunction, including reduced mitochondrial membrane potential and activities of complex I; (2) oxidative stress, including increase in reactive species, oxidative DNA damage and protein oxidation, and (3) Parkinsonism parameters, including accumulation of alpha-synuclein and poly-ubiquitin. |
31(0,1,1,1) | Details |
| 15992171 | Kahle PJ, Haass C: The emerging utility of animal models of chronic neurodegenerative diseases. Expert Opin Ther Targets. 2001 Feb;5(1):125-32. PD is characterised by intraneuronal cytoplasmic deposits (Lewy bodies) of the PD-associated gene product alpha-synuclein. Moreover, environmental risk factors such as the pesticide rotenone have been used successfully to generate rodent models of PD. |
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| 19857570 | Kalivendi SV, Yedlapudi D, Hillard CJ, Kalyanaraman B: Oxidants induce alternative splicing of alpha-synuclein: Implications for Parkinson's disease. Free Radic Biol Med. 2010 Feb 1;48(3):377-83. Epub 2009 Oct 23. Using parkinsonism mimetics (MPP (+), rotenone) and related oxidants, we have identified an oxidant-induced alternative splicing of alpha-syn mRNA, generating a shorter isoform of alpha-syn with deleted exon-5 (112-syn). |
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| 12690311 | Broussolle E, Thobois S: [Genetic and environmental factors of Parkinson's disease] . Rev Neurol. 2002;158(122):11-23. Several chemical products used in herbicides and pesticides are similar structurally to MPTP, including paraquat, diquat and rotenone. Several large kindreds with autosomal dominant Parkinson's disease associated with mutations of alpha-synuclein gene (PARK 1) were recently described. alpha-synuclein is a constituant of Lewy bodies, the hallmark of idiopathic Parkinson's disease. |
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| 19351880 | Bayir H, Kapralov AA, Jiang J, Huang Z, Tyurina YY, Tyurin VA, Zhao Q, Belikova NA, Vlasova II, Maeda A, Zhu J, Na HM, Mastroberardino PG, Sparvero LJ, Amoscato AA, Chu CT, Greenamyre JT, Kagan VE: Peroxidase mechanism of lipid-dependent cross-linking of synuclein with cytochrome C: protection against apoptosis versus delayed oxidative stress in Parkinson disease. J Biol Chem. 2009 Jun 5;284(23):15951-69. Epub 2009 Apr 7. We discovered that alpha-synuclein (Syn) forms a triple complex with anionic lipids (such as and cytochrome c, which exerts a peroxidase activity. Co-localization of Syn with cytochrome c was detected in aggregates formed upon proapoptotic stimulation of SH-SY5Y and HeLa cells and in dopaminergic substantia nigra neurons of rotenone-treated rats. |
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| 20211259 | Bayersdorfer F, Voigt A, Schneuwly S, Botella JA: -dependent neurodegeneration in Drosophila models of familial and sporadic Parkinson's disease. Neurobiol Dis. 2010 Mar 6. Combining these flies with a chemically induced Parkinson model (rotenone) and a familial form of Parkinson (mutant alpha-synuclein) we were able to show a strong reduction of neurotoxicity and a protection of the dopaminergic neurons when cellular levels were reduced. |
31(0,1,1,1) | Details |
| 14645467 | Sherer TB, Betarbet R, Testa CM, Seo BB, Richardson JR, Kim JH, Miller GW, Yagi T, Matsuno-Yagi A, Greenamyre JT: Mechanism of toxicity in rotenone models of Parkinson's disease. J Neurosci. 2003 Nov 26;23(34):10756-64. Exposure of rats to the pesticide and complex I inhibitor rotenone reproduces features of Parkinson's disease, including selective nigrostriatal dopaminergic degeneration and alpha-synuclein-positive cytoplasmic inclusions (Betarbet et al., 2000; Sherer et al., 2003). |
31(0,1,1,1) | Details |
| 12690660 | Broussolle E, Thobois S: [Genetics and environmental factors of Parkinson disease] . Rev Neurol. 2002 Dec;158 Spec no 1:S11-23. Several chemical products used in herbicides and pesticides are similar structurally to MPTP, including paraquat, diquat and rotenone. Several large kindreds with autosomal dominant Parkinson's disease associated with mutations of alpha-synuclein gene (PARK 1) were recently described. alpha-synuclein is a constituant of Lewy bodies, the hallmark of idiopathic Parkinson's disease. |
2(0,0,0,2) | 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. |
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| 12151787 | Lehmensiek V, Tan EM, Schwarz J, Storch A: Expression of mutant alpha-synucleins enhances dopamine transporter-mediated MPP+ toxicity in vitro. Neuroreport. 2002 Jul 19;13(10):1279-83. We demonstrate that expression of all alpha-synuclein isoforms enhances toxicity of general complex I inhibition (rotenone), but only the expression of mutant alpha-synucleins induces significant increased DAT-dependent toxicity of very low concentrations of MPP+ compared to wild-type protein. |
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| 17041725 | Liu YY, Zhao HY, Zhao CL, Duan CL, Lu LL, Yang H: [Overexpression of alpha-synuclein in SH-SY5Y cells partially protected against oxidative stress induced by rotenone]. Sheng Li Xue Bao. 2006 Oct 25;58(5):421-8. |
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| 19626387 | Monti B, Gatta V, Piretti F, Raffaelli SS, Virgili M, Contestabile A: is neuroprotective in the rotenone rat model of Parkinson's disease: involvement of alpha-synuclein. Neurotox Res. 2010 Feb;17(2):130-41. Epub 2009 Jul 21. |
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| 12504863 | Sherer TB, Kim JH, Betarbet R, Greenamyre JT: Subcutaneous rotenone exposure causes highly selective dopaminergic degeneration and alpha-synuclein aggregation. Exp Neurol. 2003 Jan;179(1):9-16. |
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| 16239214 | Ved R, Saha S, Westlund B, Perier C, Burnam L, Sluder A, Hoener M, Rodrigues CM, Alfonso A, Steer C, Liu L, Przedborski S, Wolozin B: Similar patterns of mitochondrial vulnerability and rescue induced by genetic modification of alpha-synuclein, parkin, and DJ-1 in Caenorhabditis elegans. J Biol Chem. 2005 Dec 30;280(52):42655-68. Epub 2005 Oct 19. C. elegans lines with these genetic changes were more vulnerable than nontransgenic nematodes to mitochondrial complex I inhibitors, including rotenone, fenperoximate, pyridaben, or stigmatellin. |
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| 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 . Synphilin-1 has been identified as an interaction partner of alpha-synuclein. |
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