Na+ CP type Vα CRISPR Activation Plasmid (h): sc-402162-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Na+ CP type Vα CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Na+ CP type Vα CRISPR Activation Plasmid (h) 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 Vα CRISPR Activation Plasmid (h) and Na+ CP type Vα CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SCN5A transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Na+ CP type Vα Antibody (H-10): sc-271255
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Na+ CP type Vα CRISPR Activation Plasmid (h) | sc-402162-ACT | 20 µg | $397.00 |
SCN5A encodes the pore-forming α subunit of the voltage-gated sodium channel Na⁺ CP type Vα (NaV1.5), a key determinant of rapid depolarization and action potential initiation in excitable cells. By mediating inward Na⁺ currents, NaV1.5 regulates membrane excitability, conduction velocity, and coupling of electrical activity to downstream Ca²⁺ handling and excitation–contraction processes. SCN5A function integrates with ion homeostasis networks and signaling pathways that influence channel trafficking, phosphorylation-dependent gating, and stress-responsive electrical remodeling. Genetic and regulatory perturbations in SCN5A are associated with inherited and acquired arrhythmia susceptibility, making it a central target for mechanistic studies of sodium current dynamics and electrophysiology-linked phenotypes.
Na+ CP type Vα CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SCN5A expression without altering the underlying DNA sequence.
Na+ CP type Vα CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SCN5A 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 SCN5A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Na+ CP type Vα expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SCN5A locus and enabling the study of Na+ CP type Vα-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 Vα pathway restoration in tumor cells with silenced or reduced SCN5A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.