| http://purl.uniprot.org/citations/17097639 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17097639 | http://www.w3.org/2000/01/rdf-schema#comment | "Expansion of the polyQ repeat in ataxin-2 results in degeneration of Purkinje neurons and other neuronal groups including the substantia nigra in patients with spinocerebellar ataxia type 2 (SCA2). In animal and cell models, overexpression of mutant ataxin-2 induces cell dysfunction and death, but little is known about steady-state levels of normal and mutant ataxin-2 and cellular mechanisms regulating their abundance. Based on preliminary findings that ataxin-2 interacted with parkin, an E3 ubiquitin ligase mutated in an autosomal recessive form of Parkinsonism, we sought to determine whether parkin played a role in regulating the steady-state levels of ataxin-2. Parkin interacted with the N-terminal half of normal and mutant ataxin-2, and ubiquitinated the full-length form of both wild-type and mutant ataxin-2. Parkin also regulated the steady-state levels of endogenous ataxin-2 in PC12 cells with regulatable parkin expression. Parkin reduced abnormalities in Golgi morphology induced by mutant ataxin-2 and decreased ataxin-2 induced cytotoxicity. In brains of SCA2 patients, parkin labeled cytoplasmic ataxin-2 aggregates in Purkinje neurons. These studies suggest a role for parkin in regulating the intracellular levels of both wild-type and mutant ataxin-2, and in rescuing cells from ataxin-2-induced cytotoxicity. The role of parkin variants in modifying the SCA2 phenotype and its use as a therapeutic target should be further investigated."xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.expneurol.2006.09.009"xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/author | "Nguyen D.T."xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/author | "Brice A."xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/author | "Pulst S.M."xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/author | "Huynh D.P."xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/author | "Pulst-Korenberg J.B."xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/name | "Exp Neurol"xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/pages | "531-541"xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/title | "Parkin is an E3 ubiquitin-ligase for normal and mutant ataxin-2 and prevents ataxin-2-induced cell death."xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://purl.uniprot.org/core/volume | "203"xsd:string |
| http://purl.uniprot.org/citations/17097639 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17097639 |
| http://purl.uniprot.org/citations/17097639 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17097639 |
| http://purl.uniprot.org/uniprot/Q99700#attribution-F898C6DB348B3A0EC03EEF9757B31329 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/17097639 |
| http://purl.uniprot.org/uniprot/O60260#attribution-F898C6DB348B3A0EC03EEF9757B31329 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/17097639 |