Date published: 2026-7-10

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αENaC Double Nickase Plasmid (m): sc-422825-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • αENaC Double Nickase Plasmid (m) 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
  • αENaC Double Nickase Plasmid (m) and αENaC Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Scnn1a. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    αENaC Double Nickase Plasmid (m)

    sc-422825-NIC
    20 µg
    $410.00

    αENaC Double Nickase Plasmid (m2)

    sc-422825-NIC-2
    20 µg
    $410.00

    Scnn1a encodes the mouse epithelial sodium channel alpha subunit (αENaC), a core pore-forming component of ENaC that mediates amiloride-sensitive Na⁺ absorption across epithelia. αENaC-dependent sodium flux contributes to transepithelial ion transport, osmotic water movement, and regulation of membrane potential in kidney, airway, and other epithelial tissues. ENaC activity is tightly controlled by proteolytic processing and ubiquitin-dependent turnover, including modulation by NEDD4L and SGK1 signaling in response to hormones such as aldosterone. Dysregulated ENaC function is associated with altered salt and fluid homeostasis and is widely studied in models of pulmonary airway surface hydration and renal sodium handling.

    αENaC Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Scnn1a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Scnn1a. 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 Scnn1a 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 Scnn1a-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.