
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
alpha Synuclein Lentiviral Activation Particles (h) | sc-417273-LAC | 200 µl | $455.00 |
SNCA encodes human alpha synuclein, a presynaptic protein implicated in synaptic vesicle trafficking, neurotransmitter release, and activity-dependent plasticity. Alpha synuclein associates with lipid membranes and can influence vesicle docking and fusion dynamics, linking it to pathways governing proteostasis, endolysosomal handling, and autophagy. Dysregulation of SNCA expression or conformational state is closely associated with Lewy body pathology and neurodegenerative mechanisms involving mitochondrial stress, oxidative damage, and neuroinflammation. These features make SNCA a widely used target for modeling neuronal vulnerability, proteotoxic stress responses, and circuit-level perturbations in cellular systems.
alpha Synuclein Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient SNCA upregulation across a broader range of human cell types.
alpha Synuclein Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the SNCA transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous alpha Synuclein expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SNCA genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.