ArticleJournal of molecular neuroscience : MN2010
Establishment of stably transfected rat neuronal cell lines expressing alpha-synuclein GFP fusion proteins.
Article in Journal of molecular neuroscience : MN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- α-Synuclein binds to the ER-mitochondria tethering protein VAPB to disrupt CaActa neuropathologica · 2017Article
- Chemical constituents of tobacco smoke induce the production of interleukin-8 in human bronchial epithelium, 16HBE cells.Tobacco induced diseases · 2016Article
- Quantitative analysis of α-synuclein solubility in living cells using split GFP complementation.PloS one · 2012Article
- In vivo imaging of alpha-synuclein in mouse cortex demonstrates stable expression and differential subcellular compartment mobility.PloS one · 2010Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the alpha-synuclein gene have been linked to rare cases of familial Parkinson's disease (PD). alpha-Synuclein, a 140 amino acid polypeptide, is a major component of Lewy bodies (LB), a pathological hallmark of PD. Transgenic mice, Drosophila and marmosets (Challitrix jacchus) expressing either wild type (WT) or mutant human alpha-synuclein develop motor deficits, LB-like inclusions in some neurons and neuronal degeneration. The effects of human alpha-synuclein were investigated in a neuronal rat cell line (B103). Plasmids expressing WT and mutant human alpha-synuclein regulated by the cytomegalovirus (CMV) promoter were prepared and used for creating stably transfected neuronal rat cell lines. For localizing alpha-synuclein expression, stably transfected neuronal rat cell lines, expressing alpha-synuclein enhanced green fluorescent protein fusion proteins, regulated by either the CMV or the human platelet-derived growth factor ss promoter were generated. Over-expression of WT and A53T alpha-synuclein regulated by CMV promoter in stable transfectants resulted in formation of alpha-synuclein-immunopositive inclusion-like structures and mitochondrial alterations. Taken together, these results suggest that abnormal accumulation of alpha-synuclein could lead to mitochondrial alterations that might result in oxidative stress and eventually, cell death.
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