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Proteins and Peptides

Alpha Synuclein A53T Mutant Monomers (Type 1)

Product Sizes
100 ug
SPR-325-100UG
2 x 100 ug
SPR-325-2X100UG
5 x 100 ug
SPR-325-5X100UG
About this Product
SKU:
SPR-325
Additional Names:
Alpha-synuclein A53T, A53T mutant alpha-synuclein, A53T mutated SNCA, Ala53Thr mutant alpha-synuclein, Asyn, SNCA, NACP, PARK1, PARK4, PD1, Synuclein alpha, Non-A beta component of AD amyloid, Non-A4 component of amyloid precursor, Synuclein Alpha-140, SYN, Parkinson's disease familial 1 Protein
Application:
Cell-based/Functional Assay, SDS-PAGE, Western Blot
Buffer:
PBS
CE/IVD:
RUO
Concentration:
2 mg/ml
Extra Details:
Alpha-synuclein (A Alpha-syn), encoded by the SNCA gene, is a neuronal protein predominantly localized at presynaptic terminals, where it regulates synaptic vesicle trafficking, neurotransmitter release, and SNARE-complex assembly. In its monomeric form, A Alpha-syn plays a crucial role in maintaining synaptic integrity and cognitive function. The A53T mutation in A Alpha-syn, characterized by a substitution of alanine with threonine at position 53, is linked to familial early-onset Parkinson's disease. This missense mutation alters the biophysical properties of A Alpha-syn monomers, increasing their propensity to misfold and aggregate into toxic oligomers and fibrils. These aggregates disrupt neuronal homeostasis, impair mitochondrial function, and trigger neuroinflammatory responses, contributing to progressive neurodegeneration. Studies have shown that A53T mutant monomers exhibit enhanced fibrillization kinetics and altered interactions with cellular components, including microtubules and SNARE proteins. Additionally, the mutation compromises A Alpha-syn's ability to regulate exocytotic fusion pore dynamics, a function critical for neurotransmitter release. The A53T variant also influences proteolytic processing, generating truncated peptides that exacerbate neurotoxicity without forming classical Lewy body aggregates. Understanding the molecular mechanisms by which A53T mutant monomers drive pathology is essential for developing targeted therapies. Interventions aimed at stabilizing monomeric A Alpha-syn, preventing aggregation, or modulating its interactions with cellular machinery offer promising avenues for mitigating disease progression in Parkinson's and related synucleinopathies.
Immunogen:
Alpha Synuclein A53T Monomers
Molecular Weight:
~14.46 kDa
Purity:
>95%
Purification:
Ion Exchange
Sequence:
MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVTTVAEKTK EQVTNVGGAV VTGVTAVAQK TVEGAGSIAA ATGFVKKDQL GKNEEGAPQE GILEDMPVDP DNEAYEMPSE EGYQDYEPEA
Shipping Conditions:
Dry Ice
Storage Conditions:
-70[o]C
Supplier:
StressMarq Biosciences
Type:
Proteins, Peptides, Small Molecules & Other Biomolecules: Recombinant Proteins
SDS-PAGE of ~14 kDa A53T Alpha Synuclein Monomer (SPR-325)
Thioflavin T is a fluorescent dye that binds to beta sheet-rich structures such as those in alpha synuclein fibrils. Upon binding, the emission spectrum of the dye experiences a red-shift and increased fluorescence intensity. Thioflavin T emission curves show a limited increase in fluorescence (correlated to alpha synuclein aggregation) over time in A53T alpha synuclein monomers (SPR-325). A much greater increase in fluorescence is seen when 100 uM monomer (SPR-325) is combined with 10 nM of fibrils (SPR-326) as the fibrils seed the formation of new fibrils from the pool of active monomers. Thioflavin T ex = 450 nm, em = 485 nm.