| Storage Buffer | PBS pH 7.4 |
| Storage Temperature | -80ºC |
| Shipping Temperature | Dry Ice. Shipping note: Product will be shipped separately from other products purchased in the same order. |
| Purification | Ion-exchange Purified |
| Cite This Product | Mouse Recombinant Alpha Synuclein Monomers (StressMarq Biosciences | Victoria, BC CANADA | Catalog# SPR-323) |
| Certificate of Analysis | Certified >95% pure using SDS-PAGE analysis. Low endotoxin <5 EU/mL @ 2mg/mL. |
| Other Relevant Information | For corresponding PFFs, see catalog# SPR-324 |
| Alternative 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 |
| Research Areas | Alzheimer's Disease, Neurodegeneration, Neuroscience, Parkinson's Disease, Synuclein, Tangles & Tau, Multiple System Atrophy |
| Cellular Localization | Cytoplasm, Membrane, Nucleus |
| Accession Number | NP_001035916.1 |
| Gene ID | 20617 |
| Swiss Prot | O55042 |
| Scientific Background |
Alpha-synuclein (α-syn), a 140-amino acid neuronal protein encoded by the SNCA gene, plays a vital role in maintaining synaptic function. In its monomeric form, α-syn regulates synaptic vesicle trafficking, neurotransmitter release, and SNARE-complex assembly, contributing to efficient neuronal communication and dopamine homeostasis. Under physiological conditions, α-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 α-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 α-syn monomers before aggregation occurs offers a promising therapeutic strategy. Approaches such as molecular chaperones, SNCA gene modulation, and immunotherapies aim to stabilize monomeric α-syn or prevent its pathological conversion. As research advances, understanding the molecular behavior of α-syn monomers is essential for developing disease-modifying treatments and biomarkers for early diagnosis in neurodegenerative disorders. |
| References |
1. “Genetics Home Reference: SNCA”. US National Library of Medicine. (2013). 2. Zhang L., et al. (2008) Brain Res. 1244: 40-52. 3. Alim M.A., et al. (2002) J Biol Chem. 277(3): 2112-2117. 4. Kokhan V.S., Afanasyeva M.A., Van'kin G. (2012) Behav. Brain. Res. 231(1): 226-230. 5. Spillantini M.G., et al. (1997) Nature. 388(6645): 839-840. 6. Mezey E., et al. (1998) Nat Med. 4(7): 755-757. |
Type 1 alpha synuclein pre-formed fibrils (SPR-324) seed the formation of new alpha synuclein fibrils from the pool of alpha synuclein monomers (SPR-323). 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 increased fluorescence (correlated to alpha synuclein protein aggregation) over time when 10 µM of Type 1 alpha synuclein pre-formed fibrils (SPR-324) is combined with 100 µM of alpha synuclein monomer (SPR-323), as compared to Type 1 alpha synuclein pre-formed fibrils (SPR-324) or alpha synuclein monomer (SPR-323) alone. Thioflavin T ex = 450 nm, em = 485 nm.
C57/BL6 mice were injected with sonicated recombinant mouse alpha synuclein monomers or fibrils at 8 weeks of age. Mice were unilaterally injected in the dorsal striatum (bregma AP + 0.2 mm, L +/1 2.0 mm, V – 3.0 mm) and sacrificed 30 days post-injection. (A) 1.25 uL mouse alpha synuclein monomers (SPR-323). (B) 2.5 uL mouse alpha synuclein monomers (SPR-323). (C) 2.5 ug alpha synuclein PFFs (SPR-324). (C) 5 ug alpha synuclein PFFs (SPR-324) Inset: PBS (negative control). Primary antibody: Anti-Alpha Synuclein pSer129 (SMC-600) at 1:10 000. Secondary antibody: anti-rabbit HRP. Mice injected with PFF displayed alpha synuclein staining in the striatum and cortex and contralateral to the injection site. Courtesy of: Porsolt.
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