Na+ CP type IIIα CRISPR Activation Plasmid (m): sc-422820-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Na+ CP type IIIα CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Na+ CP type IIIα CRISPR Activation Plasmid (m) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by Na+ CP type IIIα CRISPR Activation Plasmid (m) and Na+ CP type IIIα CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Scn3a transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Na+ CP type IIIα CRISPR Activation Plasmid (m) | sc-422820-ACT | 20 µg | $397.00 | |||
Na+ CP type IIIα CRISPR Activation Plasmid (m2) | sc-422820-ACT-2 | 20 µg | $397.00 |
Scn3a encodes the voltage-gated sodium channel alpha subunit Na+ CP type IIIα (Nav1.3), a pore-forming membrane protein that initiates and propagates action potentials by mediating rapid sodium influx. In mouse neurons, Nav1.3 contributes to intrinsic excitability and spike timing, interfacing with electrical signaling programs that coordinate synaptic transmission and neuronal network activity. SCN3A-regulated sodium currents influence activity-dependent processes such as neurite outgrowth and circuit maturation, and altered channel expression or gating has been linked to neurodevelopmental and seizure-related phenotypes. As a result, Scn3a is widely studied in models of excitability disorders, sensory processing, and neuronal differentiation.
Na+ CP type IIIα CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Scn3a expression without altering the underlying DNA sequence.
Na+ CP type IIIα CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Scn3a 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 Scn3a transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Na+ CP type IIIα expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Scn3a locus and enabling the study of Na+ CP type IIIα-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Na+ CP type IIIα pathway restoration in tumor cells with silenced or reduced Scn3a expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.