| Name | brains |
|---|---|
| Synonyms | BPG dependent PGAM 1; Brain; CDABP0006; PGAM 1; PGAM B; PGAM1; PGAM1 protein; PGAMA… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. Lewy bodies in the brains of patients with Parkinson's disease (PD) contain aggregates of alpha-synuclein (alpha-syn). |
1(0,0,0,1) | Details |
| 8250391 | Lindsay DS, Mitschler RR, Toivio-Kinnucan MA, Upton SJ, Dubey JP, Blagburn BL: Association of host cell mitochondria with developing Toxoplasma gondii tissue cysts. Am J Vet Res. 1993 Oct;54(10):1663-7. Incubation of tissue cysts from cultured cells and tissue cysts from mouse brains with rhodamine 123 revealed fluorescence of the tissue cyst wall in living specimens. Incubation of tissue cysts with 10 microM rotenone caused diminished fluorescence of the tissue cyst walls, and 100 microM rotenone caused complete inhibition. |
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. Studies of PD brains suggest that mitochondrial impairment and oxidative stress may contribute to the pathogenesis of sporadic PD. 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 |
| 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. Reactive species and advanced glycation end products (AGEs) have been found in the intracellular, alpha-synuclein-positive Lewy bodies in the brains of both PD as well as incidental Lewy body disease patients, suggesting a role for AGEs in alpha-synuclein cross-linking and Lewy body formation. 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. |
1(0,0,0,1) | Details |
| 16565515 | Jin J, Hulette C, Wang Y, Zhang T, Pan C, Wadhwa R, Zhang J: Proteomic identification of a stress protein, mortalin/mthsp70/GRP75: relevance to Parkinson disease. Mol Cell Proteomics. 2006 Jul;5(7):1193-204. Epub 2006 Mar 24. We confirmed that one of these, mortalin (mthsp70/GRP75, a mitochondrial stress protein), is substantially decreased in PD brains as well as in a cellular model of PD. |
1(0,0,0,1) | Details |
| 7561883 | Sabri MI, Lystrup B, Roy DN, Spencer PS: Action of beta-N-oxalylamino- on mouse brain NADH-dehydrogenase activity. J Neurochem. 1995 Oct;65(4):1842-8. Two known inhibitors (rotenone and 1-methyl-4-phenylpyridinium ion, MPP+) of this mitochondrial enzyme produced significant inhibition under identical conditions. |
0(0,0,0,0) | Details |
| 18804145 | Kaneko K, Hineno A, Yoshida K, Ikeda S: Increased vulnerability to rotenone-induced neurotoxicity in ceruloplasmin-deficient mice. Neurosci Lett. 2008 Nov 28;446(1):56-8. Epub 2008 Sep 11. Immunohistochemical examination showed that acrolein, one of the products of lipid peroxides, and ubiquitin were more markedly immunoreacted in the brains of rotenone-treated, Cp-deficient mice than in rotenone-untreated, Cp-deficient or rotenone-treated, wild-type mice. |
38(0,1,2,3) | Details |
| 19120153 | Moldzio R, Piskernik C, Radad K, Rausch WD: Rotenone damages striatal organotypic slice culture. Ann N Y Acad Sci. 2008 Dec;1148:530-5. Organotypic striatal slice cultures were prepared from brains of adult mice and treated with rotenone (0.01, 0.05, 0.1, and 1 mM) for 48 h. |
6(0,0,1,1) | 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. Finally, brains from rotenone-treated animals demonstrated oxidative damage, most notably in midbrain and olfactory bulb, dopaminergic regions affected by Parkinson's disease. |
6(0,0,1,1) | Details |
| 19479992 | Richter F, Meurers BH, Zhu C, Medvedeva VP, Chesselet MF: Neurons express hemoglobin alpha- and beta-chains in rat and human brains. . J Comp Neurol. 2009 Aug 10;515(5):538-47. Systemic administration of the mitochondrial inhibitor rotenone (2 mg/kg/d, 7d, s.c.) induced a marked decrease in Hba-a2 and Hbb but not neuroglobin or cytoglobin mRNA in transcriptome analyses of nigral dopaminergic neurons. |
2(0,0,0,2) | Details |
| 4009171 | Gonatas JO, Gonatas NK, Stieber A, Fleischer B: Isolation and characterization of an enriched Golgi fraction from neurons of developing rat brains. J Neurochem. 1985 Aug;45(2):497-507. The activities of the possible marker enzymes rotenone-insensitive -cytochrome c reductase, -cytochrome c reductase, and arylsulfatase were low or minimally elevated in the Golgi fractions. |
2(0,0,0,2) | Details |
| 10370869 | Zini R, Morin C, Bertelli A, Bertelli AA, Tillement JP: Effects of on the rat brain respiratory chain. Drugs Exp Clin Res. 1999;25(2-3):87-97. The aim of this work was to investigate the possible effects of on the mitochondrial respiratory chain in rat brains. The rate of consumption by the different complexes was checked using rotenone (2 microM), (10 mM), antimycin A (1 microM), (KCN) (0.3 mM) and oligomycin (10 microM) to inhibit complexes II, III, IV, V and I, respectively. |
1(0,0,0,1) | 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. This study found that both LC3-II and beclin were significantly increased in brains from humans with Dementia with Lewy bodies and transgenic mice overexpressing mutant alpha-synuclein, as compared with respective controls, suggesting that macroautophagy is induced to remove alpha-syn, particularly oligomeric or mutant forms. Finally, rotenone-induced alpha-syn aggregates were cleared following rapamycin stimulation of autophagy. |
1(0,0,0,1) | Details |
| 15066675 | Gibbs JP, Adeyeye MC, Yang Z, Shen DD: uptake by bovine brain microvessel endothelial cells: role of active efflux transport. Epilepsy Res. 2004 Jan;58(1):53-66. Brain microvessel endothelial cells (BMEC) were isolated from cow brains and grown to confluence. |
1(0,0,0,1) | Details |
| 2176115 | Dagani F, Ferrari R, Canevari L: A pharmacological model for studying the role of Na+ gradients in the modulation of synaptosomal free [Ca2+] i levels and energy metabolism. Brain Res. 1990 Oct 22;530(2):261-6. Lactate production (Jlac), consumption rate (QO2), plasma membrane potentials (Em) and cytosolic free levels [Ca2+] i were studied on synaptosomes isolated from rat brains, incubated in presence of high doses of nicardipine (90 microM), (0.5 mM) and (0.25 mM), and submitted to depolarizing stimulation or inhibition of mitochondrial respiration. Synaptosomes were also submitted to an inhibition of respiration of intrasynaptic mitochondria by incubation with rotenone (5 microM); in this condition of mimicked hypoxia Em was more positive of about 11 mV; none of the drugs utilized modified this situation. |
1(0,0,0,1) | Details |
| 17005863 | Malagelada C, Ryu EJ, Biswas SC, Jackson-Lewis V, Greene LA: RTP801 is elevated in Parkinson brain substantia nigral neurons and mediates death in cellular models of Parkinson's disease by a mechanism involving mammalian target of rapamycin inactivation. J Neurosci. 2006 Sep 27;26(39):9996-10005. To assess the relevance of these observations to PD, we used immunohistochemistry to compare RTP801 expression in postmortem brains from PD and control patients. |
1(0,0,0,1) | Details |
| 16750479 | Sharma SK, El Refaey H, Ebadi M: Complex-1 activity and 18F- uptake in genetically engineered mouse model of Parkinson's disease and the neuroprotective role of Brain Res Bull. 2006 Jun 15;70(1):22-32. Epub 2005 Dec 27. Regional distribution of and mitochondrial complex-1 activity were estimated in the brains of control-(C57BL/6), metallothionein knock out-, metallothionein transgenic-, and homozygous weaver mutant mice; and human dopaminergic (SK-N-SH) cells with a primary objective to determine the neuroprotective potential of in Parkinson's disease. Direct exposure of rotenone also reduced coenzyme Q10, complex-1 activity, and mitochondrial membrane potential in SK-N-SH cells. |
1(0,0,0,1) | Details |