| 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 | paraquat |
|---|---|
| CAS | 1,1′-dimethyl-4,4′-bipyridinium |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11707429 | Manning-Bog AB, McCormack AL, Li J, Uversky VN, Fink AL, Di Monte DA: The herbicide paraquat causes up-regulation and aggregation of alpha-synuclein in mice: paraquat and alpha-synuclein. J Biol Chem. 2002 Jan 18;277(3):1641-4. Epub 2001 Nov 13. Because pesticides, particularly the herbicide paraquat, have been suggested to play a role as PD risk factors, the hypothesis that interactions between alpha-synuclein and these environmental agents may contribute to aggregate formation was tested in this study. |
104(1,1,4,9) | Details |
| 19101702 | Chau KY, Korlipara LV, Cooper JM, Schapira AH: Protection against paraquat and A53T alpha-synuclein toxicity by cabergoline is partially mediated by receptors. J Neurol Sci. 2009 Mar 15;278(1-2):44-53. Epub 2008 Dec 21. |
93(0,3,3,3) | Details |
| 16321246 | Du YL, Liu ZG, Chen SD, Lu GQ: [Effects of different doses of on paraquat-induced neurotoxicity: an experiment with mice]. Zhonghua Yi Xue Za Zhi. 2005 Sep 7;85(34):2400-3. CONCLUSION: Pre-treatment with lower dose before the paraquat administration is neuroprotective by preventing paraquat from access into central nervous system through a blood-brain barrier competitive uptake mechanism, while higher dose shows neurotoxicity through disaggregating alpha-synuclein deposits in Parkinsonian mice. |
87(1,1,2,2) | Details |
| 17934957 | Yang W, Tiffany-Castiglioni E: The bipyridyl herbicide paraquat induces proteasome dysfunction in human neuroblastoma SH-SY5Y cells. J Toxicol Environ Health A. 2007 Nov;70(21):1849-57. Furthermore, levels of alpha-synuclein and ubiquitin-conjugated proteins were measured to test whether paraquat induces protein accumulation in SY5Y cells. |
87(1,1,2,2) | Details |
| 12716914 | Manning-Bog AB, McCormack AL, Purisai MG, Bolin LM, Di Monte DA: Alpha-synuclein overexpression protects against paraquat-induced neurodegeneration. J Neurosci. 2003 Apr 15;23(8):3095-9. In control mice, paraquat caused both the formation of alpha-synuclein-containing intraneuronal deposits and the degeneration of nigrostriatal neurons, as demonstrated by silver staining and a reduction of the counts of TH-positive and Nissl-stained cells. |
64(0,1,6,9) | Details |
| 17879265 | Fernagut PO, Hutson CB, Fleming SM, Tetreaut NA, Salcedo J, Masliah E, Chesselet MF: Behavioral and histopathological consequences of paraquat intoxication in mice: effects of alpha-synuclein over-expression. Synapse. 2007 Dec;61(12):991-1001. |
30(0,0,5,5) | Details |
| 20200163 | Mak SK, McCormack AL, Manning-Bog AB, Cuervo AM, Di Monte DA: Lysosomal degradation of {alpha}-synuclein in vivo. J Biol Chem. 2010 Mar 3. When neuronal alpha-synuclein expression was enhanced as a result of toxic injury (i.e. treatment of mice with the herbicide paraquat) or transgenic protein overexpression, the intralysosomal content of alpha-synuclein was also significantly increased. |
18(0,0,2,8) | Details |
| 15234109 | Orth M, Tabrizi SJ, Tomlinson C, Messmer K, Korlipara LV, Schapira AH, Cooper JM: G209A mutant alpha synuclein expression specifically enhances induced oxidative damage. Neurochem Int. 2004 Oct;45(5):669-76. We have induced G209A mutant or wild-type alpha-synuclein expression in stable HEK293 cell models to determine if this influences markers of oxidative stress and damage under normal conditions or in the presence of or paraquat. |
16(0,0,2,6) | Details |
| 16756753 | Choi HS, Lee SH, Kim SY, An JJ, Hwang SI, Kim DW, Yoo KY, Won MH, Kang TC, Kwon HJ, Kang JH, Cho SW, Kwon OS, Choi JH, Park J, Eum WS, Choi SY: Transduced Tat-alpha-synuclein protects against oxidative stress in vitro and in vivo. J Biochem Mol Biol. 2006 May 31;39(3):253-62. WT Tat-alpha-synuclein rapidly transduced into an astrocyte cells and protected the cells against paraquat induced cell death. |
11(0,0,1,6) | Details |
| 12859192 | Goers J, Manning-Bog AB, McCormack AL, Millett IS, Doniach S, Di Monte DA, Uversky VN, Fink AL: Nuclear localization of alpha-synuclein and its interaction with histones. Biochemistry. 2003 Jul 22;42(28):8465-71. We also describe the presence of alpha-synuclein and its co-localization with histones in the nuclei of nigral neurons from mice exposed to a toxic insult (i.e., injections of the herbicide paraquat). |
10(0,0,1,5) | 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 |
| 17255333 | Norris EH, Uryu K, Leight S, Giasson BI, Trojanowski JQ, Lee VM: Pesticide exposure exacerbates alpha-synucleinopathy in an A53T transgenic mouse model. Am J Pathol. 2007 Feb;170(2):658-66. In this study, A53T mutant human alpha-synuclein transgenic mice (M83), which develop alpha-synuclein neuropathology, were treated with the pesticides paraquat and maneb (either singly or together), and their effects were analyzed. |
8(0,0,1,3) | Details |
| 12641729 | McCormack AL, Di Monte DA: Effects of and other amino acids against paraquat-induced nigrostriatal degeneration. J Neurochem. 2003 Apr;85(1):82-6. Exposure to the herbicide paraquat causes selective nigrostriatal degeneration and aggregation of alpha-synuclein in the mouse brain. |
6(0,0,1,1) | Details |
| 15362105 | Munishkina LA, Cooper EM, Uversky VN, Fink AL: The effect of macromolecular crowding on protein aggregation and amyloid fibril formation. J Mol Recognit. 2004 Sep-Oct;17(5):456-64. In this report we summarize data demonstrating that macromolecular crowding may lead to a dramatic acceleration in the rate of protein aggregation and formation of amyloid fibrils, using the protein alpha-synuclein. |
4(0,0,0,4) | 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 |
| 15009131 | Thiruchelvam MJ, Powers JM, Cory-Slechta DA, Richfield EK: Risk factors for dopaminergic neuron loss in human alpha-synuclein transgenic mice. Eur J Neurosci. 2004 Feb;19(4):845-54. Treatment with Mn2+-ethylenebisdithiocarbamate and paraquat resulted in significantly greater effects in the double-mutant line than the other lines. |
5(0,0,0,5) | Details |
| 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. In contrast, the genetic manipulations did not increase sensitivity to paraquat, azide, divalent metal ions (Fe (II) or Cu (II)), or etoposide compared with the nontransgenic nematodes. |
2(0,0,0,2) | 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. |
2(0,0,0,2) | Details |
| 16815551 | Dinis-Oliveira RJ, Remiao F, Carmo H, Duarte JA, Navarro AS, Bastos ML, Carvalho F: Paraquat exposure as an etiological factor of Parkinson's disease. Neurotoxicology. 2006 Dec;27(6):1110-22. Epub 2006 Jul 3. The role of genetic predisposition in PD has been increasingly acknowledged and a number of relevant genes have been identified (e.g., genes encoding alpha-synuclein, parkin, and dardarin), while the search for environmental factors that influence the pathogenesis of PD has only recently begun to escalate. |
1(0,0,0,1) | Details |
| 16962931 | Choi HS, An JJ, Kim SY, Lee SH, Kim DW, Yoo KY, Won MH, Kang TC, Kwon HJ, Kang JH, Cho SW, Kwon OS, Park J, Eum WS, Choi SY: PEP-1-SOD fusion protein efficiently protects against paraquat-induced dopaminergic neuron damage in a Parkinson disease mouse model. Free Radic Biol Med. 2006 Oct 1;41(7):1058-68. Epub 2006 Jun 15. This protective effect was synergistically increased when the PEP-1-SOD was cotransduced with Tat-alpha-synuclein. |
1(0,0,0,1) | Details |
| 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. |
2(0,0,0,2) | Details |
| 18056701 | Fei Q, McCormack AL, Di Monte DA, Ethell DW: Paraquat neurotoxicity is mediated by a Bak-dependent mechanism. . J Biol Chem. 2008 Feb 8;283(6):3357-64. Epub 2007 Dec 4. Oxidative stress, c-Jun N-terminal kinase activation, and alpha-synuclein aggregation are each induced by PQ, but details of the cell death mechanisms involved remain unclear. |
1(0,0,0,1) | 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 |
| 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 |