| http://purl.uniprot.org/citations/24613828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24613828 | http://www.w3.org/2000/01/rdf-schema#comment | "Hypoxic/ischemic brain injury is a potential cause of Parkinson's disease (PD) with ɑ-synuclein playing a critical role in the pathophysiology. Since δ-opioid receptor (DOR) is neuroprotective against hypoxic/ischemic insults, we sought to determine if DOR regulates ɑ-synuclein under hypoxia and/or MPP(+) stress. We found that in HEK293 cells 1) MPP(+) in normoxia enhanced ɑ-synuclein expression and the formation of ɑ-synuclein oligomers thereby causing cytotoxic injury; 2) hypoxia at 1% O2 for 48h or at 0.5% O2 for 24h also induced ɑ-synuclein overexpression and its oligomer formation with cell injury; 3) however, hypoxia at 1% O2 for 24h, though increasing ɑ-synuclein expression, did not cause ɑ-synuclein oligomer formation and cell injury; 4) UFP-512 mediated DOR activation markedly attenuated the hypoxic cell injury and ɑ-synuclein overexpression, which was largely attenuated by DOR antagonism with naltrindole or siRNA "knock-down" of the DOR; and 5) DOR activation enhanced CREB phosphorylation and prevented the collapse of mitochondrial membrane potential (△ψm). These findings suggest that DOR activation attenuates MPP(+) or severe hypoxia induced ɑ-synuclein expression/aggregation via a CREB pathway."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.expneurol.2014.02.022"xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Chen T."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Xia Y."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Zhao J."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Wen G."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Liao X."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Sandhu H.K."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/author | "Chao D."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/name | "Exp Neurol"xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/pages | "127-136"xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/title | "delta-Opioid receptor activation reduces alpha-synuclein overexpression and oligomer formation induced by MPP(+) and/or hypoxia."xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://purl.uniprot.org/core/volume | "255"xsd:string |
| http://purl.uniprot.org/citations/24613828 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24613828 |
| http://purl.uniprot.org/citations/24613828 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24613828 |
| http://purl.uniprot.org/uniprot/P41143#attribution-138B61797C02F8007D9F35EC6DFB862B | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/24613828 |
| http://purl.uniprot.org/uniprot/P41143#attribution-59EA9D2784341E88D5B9E54F635F3077 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/24613828 |