
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SV2A CRISPR Activation Plasmid (m) | sc-425665-ACT | 20 µg | $397.00 |
Mouse Sv2a encodes synaptic vesicle glycoprotein 2A (SV2A), an integral membrane component of presynaptic vesicles that regulates vesicle priming and neurotransmitter release probability. SV2A participates in activity-dependent synaptic transmission by influencing vesicle cycling and calcium-coupled exocytosis, supporting efficient synaptic vesicle trafficking and recycling. Altered SV2A expression or function is associated with disrupted neuronal network excitability and has been used as a molecular readout in studies of epilepsy, neurodevelopmental phenotypes, and broader synaptic dysfunction relevant to neurological disease mechanisms.
SV2A CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Sv2a expression without altering the underlying DNA sequence.
SV2A CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Sv2a 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 Sv2a transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SV2A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Sv2a locus and enabling the study of SV2A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SV2A pathway restoration in tumor cells with silenced or reduced Sv2a expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.