{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rousseaux MWC"],"funding":["NICHD NIH HHS","NINDS NIH HHS","CIHR"],"pagination":["9286-9301"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6199406"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["38(43)"],"pubmed_abstract":["Accumulation of α-Synuclein (α-Syn) causes Parkinson's disease (PD) as well as other synucleopathies. α-Syn is the major component of Lewy bodies and Lewy neurites, the proteinaceous aggregates that are a hallmark of sporadic PD. In familial forms of PD, mutations or copy number variations in <i>SNCA</i> (the α-Syn gene) result in a net increase of its protein levels. Furthermore, common risk variants tied to PD are associated with small increases of <i>wild-type</i> α-Syn levels. These findings are further bolstered by animal studies which show that overexpression of α-Syn is sufficient to cause PD-like features. Thus, increased α-Syn levels are intrinsically tied to PD pathogenesis and underscore the importance of identifying the factors that regulate its levels. In this study, we establ"],"journal":["The Journal of neuroscience : the official journal of the Society for Neuroscience"],"pubmed_title":["A Druggable Genome Screen Identifies Modifiers of α-Synuclein Levels via a Tiered Cross-Species Validation Approach."],"pmcid":["PMC6199406"],"funding_grant_id":["R21 NS096395","U54 HD083092","R21 NS089854"],"pubmed_authors":["Jeong HH","Kim JJ","Shulman JM","Xu Q","Elledge SJ","Revelli JP","Westbrook TF","Bajic A","Li MZ","Kang H","Liu Z","Lavery LA","Zoghbi HY","Rousseaux MWC","Kim JY","Al-Ramahi I","Botas J","Phan ET","Perez AM","Vazquez-Velez GE","Deger JM","Ye H"],"additional_accession":[]},"is_claimable":false,"name":"A Druggable Genome Screen Identifies Modifiers of α-Synuclein Levels via a Tiered Cross-Species Validation Approach.","description":"Accumulation of α-Synuclein (α-Syn) causes Parkinson's disease (PD) as well as other synucleopathies. α-Syn is the major component of Lewy bodies and Lewy neurites, the proteinaceous aggregates that are a hallmark of sporadic PD. In familial forms of PD, mutations or copy number variations in <i>SNCA</i> (the α-Syn gene) result in a net increase of its protein levels. Furthermore, common risk variants tied to PD are associated with small increases of <i>wild-type</i> α-Syn levels. These findings are further bolstered by animal studies which show that overexpression of α-Syn is sufficient to cause PD-like features. Thus, increased α-Syn levels are intrinsically tied to PD pathogenesis and underscore the importance of identifying the factors that regulate its levels. In this study, we establ","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Oct","modification":"2026-04-07T15:23:01.63Z","creation":"2019-06-06T22:45:52Z"},"accession":"S-EPMC6199406","cross_references":{"pubmed":["30249792"],"doi":["10.1523/JNEUROSCI.0254-18.2018","10.1523/jneurosci.0254-18.2018"]}}