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SPR-505

Alpha Synuclein S129A Mutant Monomers

Cannot supply to this region.

SKU:
SPR-505
Additional Names:
Alpha-synuclein, Alpha synuclein, Non-A beta component of AD amyloid, Non-A4 component of amyloid precursor, NACP, SNCA, PARK1, SYN, PD1, PARK4, Synuclein Alpha, Parkinson's disease familial 1 Protein, Alpha Synuclein S129A, Asyn
Application:
WB, FuncS
Concentration:
2 mg/ml
Molecular Weight:
14.44 kDa
Purity:
>95%
Purification:
Ion Exchange
Storage Conditions:
-70[o]C
Supplier:
StressMarq Biosciences
ABP:
No Import Docs
Buffer:
1X PBS pH7.4
Immunogen:
Alpha Synuclein S129A Monomers
Species:
Human
Sequence:
MDVFMKGLSKAKEGVVAAAEKTKQGVAEAAGKTKEGVLYVGSKTKEGVVHGVATVAEKTKEQVTNVGGAVVTGVTAVAQKTVEGAGSIAAATGFVKKDQLGKNEEGAPQEGILEDMPVDPDNEAYEMPAEEGYQDYEPEA
Uniprot:
P37840-1
Synonyms:
Non-A beta component of AD amyloid;Non-A4 component of amyloid precursor
Extra Details:
Alpha-synuclein (A Alpha-synuclein), encoded by the SNCA gene, is a presynaptic neuronal protein involved in synaptic vesicle trafficking, neurotransmitter release, and SNARE-complex assembly. Phosphorylation at serine 129 (S129) is a hallmark of pathological A Alpha-synuclein found in Lewy bodies, the defining feature of Parkinson's disease and related synucleinopathies. The S129A mutation replaces serine with alanine, preventing phosphorylation at this critical site. This modification allows researchers to isolate the functional consequences of phosphorylation-independent A Alpha-synuclein behavior. S129A mutant monomers exhibit altered aggregation kinetics, membrane interactions, and cellular toxicity profiles, making them a valuable tool for dissecting the molecular mechanisms of A Alpha-synuclein pathology. In neurodegenerative disease models, S129A monomers help clarify the role of post-translational modifications in A Alpha-synuclein misfolding, oligomerization, and neurotoxicity. Their use enables targeted investigation into how phosphorylation influences protein conformation, intracellular trafficking, and interactions with cellular components such as mitochondria and lysosomes. By providing a phosphorylation-null background, Alpha-Synuclein S129A mutant monomers support the development of therapeutic strategies aimed at modulating A Alpha-synuclein structure and function. They are instrumental in screening compounds that prevent aggregation, enhance clearance, or restore synaptic integrity, thereby accelerating translational research in Parkinson's disease and other neurodegenerative disorders.
Shipping Conditions:
Dry Ice