Name: Mouse α-Synuclein/SNCA Recombinant Protein (His Tag)

Synonyms: Alpha-synuclein;Non-A beta component of AD amyloid;Non-A4 component of amyloid precursor;NACP;Snca

Expression host: E.coli

Sequence: Met1-Ala140

Accesstion: O55042

Species: Mouse

Mol_Mass: 15.9 kDa

AP_Mol_Mass: 18 kDa

Tag: N-His

Purity: > 95 % as determined by reducing SDS-PAGE.

Endotoxin:

Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Formulation: Lyophilized from a 0.2 μm filtered solution of 20mM PB, 150mM NaCl, pH 7.4.Normally 5 % – 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.Please refer to the specific buffer information in the printed man

Reconstitution: Please refer to the printed manual for detailed information.

Background: Alpha-synuclein (Snca) belongs to a family of proteins including a-, b-, and g-synucleins. Alpha-synuclein has been found to be implicated in the pathophysiology of many neurodegenerative diseases, including Parkinson’s disease (PD) and Alzheimer’s disease. Manyneurodegenerative diseases has shown that alpha-synuclein accumulates in dystrophic neurites and in Lewy bodies. The function of alpha-synuclein is closely correlated with its three-dimensional structure, especially for proteins important in the pathogenesis of neurodegenerative diseases. Alpha-synuclein is a dynamic molecule whose secondary structure depends on the environment. For example, it has an unfolded random coil structure in aqueous solution, forms a-helical structure upon binding to acidic phospholipid vesicles, and forms insoluble fibrils with a high b-sheet content that resemble the filaments found in Lewy bodies. Also, alpha-synuclein was known to associate with 14-3-3 proteins including protein kinase C, BAD, and extracellular regulated kinase, and overexpression of alpha-synuclein could contribute to cell death in neurodegenerative diseases.

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