gamma Synuclein/SNCG CRISPR Activation Plasmid (h): sc-401050-ACT

SNCG encodes gamma-synuclein, a small neuronal protein implicated in synaptic function, cytoskeletal dynamics, and vesicle trafficking, with broader roles in cellular stress responses. In non-neuronal contexts, gamma-synuclein has been linked to modulation of microtubule stability, protein aggregation propensity, and signaling programs that influence proliferation and migration. Dysregulated SNCG expression has been reported in multiple cancers and is frequently studied as a marker of tumor progression and metastatic potential, while also intersecting with pathways relevant to neurodegeneration. These features make SNCG a useful node for dissecting transcriptional control, proteostasis, and cytoskeleton-associated signaling networks.

gamma Synuclein/SNCG CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SNCG expression without altering the underlying DNA sequence.

gamma Synuclein/SNCG CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SNCG locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the SNCG transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous gamma Synuclein/SNCG expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SNCG locus and enabling the study of gamma Synuclein/SNCG-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of gamma Synuclein/SNCG pathway restoration in tumor cells with silenced or reduced SNCG expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.