SNCA Protein, Human

SNCA Protein is a protein abnormally aggregated to form Lewy bodies. SNCA Protein causes neuronal differentiation and maturation disorders, inhibits neurite outgrowth, reduces neuronal electrical activity through increased gene copy number (such as triploidy) or mutation, and promotes the release of extracellular toxic particles (such as oligomers) by interfering with the autophagy-lysosomal pathway (ALP), thereby inducing inflammatory responses and damage to neighboring cells. SNCA Protein, Human is a recombinant SNCA protein expressed by E. coli without a tag.

SNCA Protein belongs to the synuclein family. SNCA Protein is a protein that abnormally aggregates to form Lewy bodies^[1]. SNCA Protein causes neuronal differentiation and maturation disorders, inhibits neurite outgrowth, and reduces neuronal electrical activity through gene copy number increase (such as triploidy) or mutation. It also promotes the release of extracellular toxic particles (such as oligomers) by interfering with the autophagy-lysosomal pathway (ALP), thereby inducing inflammatory responses and neighboring cell damage^[1][2][3]. SNCA Protein is mainly expressed in neurons of the central nervous system, especially enriched in dopaminergic neurons^[1]. The normal activity of SNCA Protein is related to the dynamic regulation of synaptic vesicles and the release of neurotransmitters, but its abnormal aggregation under pathological conditions can damage mitochondrial function, induce oxidative stress, and spread toxicity between cells through exosomes and other pathways, exacerbating neurodegenerative diseases^[1][2][3]. SNCA Protein, Human is encoded by the human SNCA gene. The protein contains 140 amino acid residues, and its aggregation tendency can be affected by post-translational modifications (such as phosphorylation and ubiquitination)^[1][4].

Measured by its ability to inhibit cell proliferation of A549 cells. The ED₅₀ for this effect is typically 15.86 ng/mL, corresponding to a specific activity is 6.31×10⁴ units/mg.

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  Measured by its ability to inhibit cell proliferation of A549 cells. The ED₅₀ for this effect is typically 15.86 ng/mL, corresponding to a specific activity is 6.31×10⁴ units/mg.

Human

E. coli

Tag Free

P37840-1 (M1-A140)

6622  [NCBI]

MDVFMKGLSKAKEGVVAAAEKTKQGVAEAAGKTKEGVLYVGSKTKEGVVHGVATVAEKTKEQVTNVGGAVVTGVTAVAQKTVEGAGSIAAATGFVKKDQLGKNEEGAPQEGILEDMPVDPDNEAYEMPSEEGYQDYEPEA

Approximately 18.0 kDa

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  Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized powder.

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4 or PBS, pH 7.4, 8% trehalose.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Oliveira LM, et al. Elevated α-synuclein caused by SNCA gene triplication impairs neuronal differentiation and maturation in Parkinson's patient-derived induced pluripotent stem cells. Cell Death Dis. 2015 Nov 26;6(11):e1994.  [Content Brief]

  [2]. Poehler AM, et al. Autophagy modulates SNCA/α-synuclein release, thereby generating a hostile microenvironment. Autophagy. 2014;10(12):2171-92.  [Content Brief]

  [3]. Minakaki G, et al. Autophagy inhibition promotes SNCA/alpha-synuclein release and transfer via extracellular vesicles with a hybrid autophagosome-exosome-like phenotype. Autophagy. 2018;14(1):98-119.  [Content Brief]

  [4]. Momcilovic O, et al. Derivation, Characterization, and Neural Differentiation of Integration-Free Induced Pluripotent Stem Cell Lines from Parkinson's Disease Patients Carrying SNCA, LRRK2, PARK2, and GBA Mutations. PLoS One. 2016 May 18;11(5):e0154890.  [Content Brief]