Alpha Synuclein Monomers (Type 1)

Cannot supply to this region.

SKU:: SPR-323XE
Additional Names:: Alpha-synuclein, 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 Protein
Application:: SDS-PAGE, WB, FuncS
Molecular Weight:: ~14.46 kDa
Purity:: >95%
Purification:: Ion Exchange
Storage Conditions:: -70[o]C
Supplier:: StressMarq Biosciences
ABP:: No Import Docs
Buffer:: PBS
Immunogen:: Alpha Synuclein Monomers
Species:: Mouse
Sequence:: MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVTTVAEKTK EQVTNVGGAV VTGVTAVAQK TVEGAGNIAA ATGFVKKDQM GKGEEGYPQE GILEDMPVDP GSEAYEMPSE EGYQDYEPEA
Uniprot:: O55042
Synonyms:: al;alp;alpha-Syn;alpha-synuclein;alphaSYN;NACP;non-A beta component of AD amyloid;non-A4 component of amyloid;Non-A4 component of amyloid precursor
Extra Details:: Alpha-synuclein (A Alpha-syn), a 140-amino acid neuronal protein encoded by the SNCA gene, plays a vital role in maintaining synaptic function. In its monomeric form, A Alpha-syn regulates synaptic vesicle trafficking, neurotransmitter release, and SNARE-complex assembly, contributing to efficient neuronal communication and dopamine homeostasis. Under physiological conditions, A Alpha-syn monomers exhibit a dynamic, unfolded structure that allows interaction with lipid membranes and synaptic proteins. However, environmental stressors, genetic mutations, and aging can destabilize this native conformation, triggering misfolding and self-aggregation. These misfolded monomers act as seeds for the formation of toxic oligomers and fibrils, initiating a prion-like propagation of pathology across neural networks. This pathological transformation disrupts synaptic integrity, impairs mitochondrial function, and activates neuroinflammatory pathways, ultimately leading to neuronal death. Monomeric A Alpha-syn is increasingly recognized as a critical upstream factor in the development of synucleinopathies, including Parkinson's disease, Lewy body dementia, and multiple system atrophy. Targeting A Alpha-syn monomers before aggregation occurs offers a promising therapeutic strategy. Approaches such as molecular chaperones, SNCA gene modulation, and immunotherapies aim to stabilize monomeric A Alpha-syn or prevent its pathological conversion. As research advances, understanding the molecular behavior of A Alpha-syn monomers is essential for developing disease-modifying treatments and biomarkers for early diagnosis in neurodegenerative disorders.

Shipping Conditions:: Dry Ice