Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
αENaC CRISPR Activation Plasmid (m): sc-422825-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- αENaC CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- αENaC 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 αENaC CRISPR Activation Plasmid (m) and αENaC CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Scnn1a transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
αENaC CRISPR Activation Plasmid (m) | sc-422825-ACT | 20 µg | $397.00 |
Scnn1a encodes the mouse epithelial sodium channel alpha subunit (αENaC), a pore-forming component required for amiloride-sensitive Na⁺ transport across epithelial membranes. αENaC contributes to apical sodium uptake that influences airway surface liquid homeostasis, alveolar fluid clearance, and transepithelial electrolyte balance in kidney, lung, and distal colon. Channel activity is integrated with aldosterone signaling and protease-dependent gating, and is modulated by ubiquitin-dependent trafficking pathways such as NEDD4-2–mediated regulation. Dysregulated ENaC function is widely used as a model for altered salt and fluid handling, linking Scnn1a expression to studies of airway dehydration, mucus obstruction phenotypes, and blood pressure–related physiology in vivo and in cultured epithelia.
αENaC CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Scnn1a expression without altering the underlying DNA sequence.
αENaC CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Scnn1a 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 Scnn1a transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous αENaC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Scnn1a locus and enabling the study of αENaC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of αENaC pathway restoration in tumor cells with silenced or reduced Scnn1a expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.