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Synphilin-1 associates with alpha-synuclein and promotes the formation of cytosolic inclusions.
- Source :
-
Nature genetics [Nat Genet] 1999 May; Vol. 22 (1), pp. 110-4. - Publication Year :
- 1999
-
Abstract
- Parkinson disease (PD) is a neurodegenerative disease characterized by tremor, bradykinesia, rigidity and postural instability. Post-mortem examination shows loss of neurons and Lewy bodies, which are cytoplasmic eosinophilic inclusions, in the substantia nigra and other brain regions. A few families have PD caused by mutations (A53T or A30P) in the gene SNCA (encoding alpha-synuclein). Alpha-synuclein is present in Lewy bodies of patients with sporadic PD, suggesting that alpha-synuclein may be involved in the pathogenesis of PD. It is unknown how alpha-synuclein contributes to the cellular and biochemical mechanisms of PD, and its normal functions and biochemical properties are poorly understood. To determine the protein-interaction partners of alpha-synuclein, we performed a yeast two-hybrid screen. We identified a novel interacting protein, which we term synphilin-1 (encoded by the gene SNCAIP). We found that alpha-synuclein interacts in vivo with synphilin-1 in neurons. Co-transfection of both proteins (but not control proteins) in HEK 293 cells yields cytoplasmic eosinophilic inclusions.
- Subjects :
- Amino Acid Sequence
Animals
Brain Chemistry
Carrier Proteins genetics
Cell Line
Chromosomes, Human, Pair 5 genetics
Female
Humans
Lewy Bodies metabolism
Male
Molecular Sequence Data
Nerve Tissue Proteins genetics
Parkinson Disease genetics
Parkinson Disease metabolism
Plasmids genetics
Protein Binding
RNA, Messenger genetics
RNA, Messenger metabolism
Rats
Saccharomyces cerevisiae genetics
Sequence Homology, Amino Acid
Synucleins
Tissue Distribution
Tissue Extracts metabolism
Transfection
alpha-Synuclein
Carrier Proteins metabolism
Inclusion Bodies metabolism
Nerve Tissue Proteins metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1061-4036
- Volume :
- 22
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Nature genetics
- Publication Type :
- Academic Journal
- Accession number :
- 10319874
- Full Text :
- https://doi.org/10.1038/8820