Releasing the nerve cell killers

Nature Medicine

Volumn 8, Issue 6, 2002, Pages 564-565

  Welch, Kevin ^a   Yuan, Junying ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA SYNUCLEIN; DOPAMINE; REACTIVE OXYGEN METABOLITE;

APOPTOSIS; BIOSYNTHESIS; CELL DEATH; CELL KILLING; DOPAMINERGIC NERVE CELL; HUMAN; MUTATION; NERVE CELL; NEUROPATHOLOGY; PARKINSON DISEASE; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN ANALYSIS; PROTEIN STRUCTURE; SHORT SURVEY; SUBSTANTIA NIGRA;

14-3-3 PROTEINS; APOPTOSIS; DOPAMINE; HUMANS; NERVE TISSUE PROTEINS; NEURONS; PARKINSON DISEASE; PHOSPHOPROTEINS; SYNUCLEINS; TYROSINE 3-MONOOXYGENASE;

EID: 0036284206     PISSN: 10788956     EISSN: None     Source Type: Journal    
DOI: 10.1038/nm0602-564     Document Type: Short Survey

References (12)

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2. Mice lacking a-synuclein display functional deficits in the nigrostriatal dopamine system
3. Dopamine-dependent neurotoxicity of native α-synuclein: A mechanism for selective neurodegeneration in Parkinson disease
4. Expression of mutant α-synuclein causes increased susceptibility to dopamine toxicity
5. Overexpression of human α-synuclein causes dopamine neuron death in rat primary culture and immortalized mesencephaon-derived cells
6. Human α-synuclein over-expression increases intracellular reactive oxygen species levels and susceptibility to dopamine
7. Recent advances in the genetics and pathogenesis of Parkinson's disease
8. α-synuclein shares physical and functional homogy with 14-3- 3 proteins
9. Synphilin-1 associates with α-synuclein and promotes the formation of cytosolic inclusion
10. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
11. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor
12. 14-3-3 Proteins in Lewy bodies in Parkinson's disease and diffuse Lewy body disease brains