δENaC Double Nickase Plasmid (h): sc-404577-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- δENaC Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- δENaC Double Nickase Plasmid (h) and δENaC Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SCNN1D. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
δENaC Double Nickase Plasmid (h) | sc-404577-NIC | 20 µg | $410.00 | |||
δENaC Double Nickase Plasmid (h2) | sc-404577-NIC-2 | 20 µg | $410.00 |
SCNN1D encodes the delta subunit of the epithelial sodium channel (δENaC), a non-voltage-gated, amiloride-sensitive Na⁺ channel that contributes to transepithelial sodium absorption and membrane potential regulation. δENaC can assemble with other ENaC subunits to influence channel gating and ion selectivity, supporting electrolyte and fluid homeostasis in epithelial tissues. ENaC activity is regulated by proteolytic processing, ubiquitination by NEDD4L, and signaling inputs that affect channel trafficking and open probability, linking SCNN1D to pathways controlling epithelial transport. Altered ENaC function is implicated in disorders of salt and fluid balance and has been studied in the context of airway surface hydration and blood pressure–related phenotypes.
δENaC Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SCNN1D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SCNN1D. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt SCNN1D function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of SCNN1D-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.