Date published: 2026-7-4

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11β-HSD2 Double Nickase Plasmid (h): sc-401400-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • 11β-HSD2 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
  • 11β-HSD2 Double Nickase Plasmid (h) and 11β-HSD2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HSD11B2. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: 11β-HSD2 Antibody (C-9): sc-365529
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    11β-HSD2 Double Nickase Plasmid (h)

    sc-401400-NIC
    20 µg
    $410.00

    11β-HSD2 Double Nickase Plasmid (h2)

    sc-401400-NIC-2
    20 µg
    $410.00

    HSD11B2 encodes human 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an NAD+-dependent oxidoreductase that inactivates cortisol to cortisone and thereby protects mineralocorticoid receptor signaling from glucocorticoid excess. This enzyme is a key determinant of steroid hormone pre-receptor metabolism and contributes to electrolyte homeostasis in mineralocorticoid-responsive epithelia, including kidney and colon. Altered HSD11B2 expression or activity is linked to dysregulated corticosteroid signaling and phenotypes consistent with apparent mineralocorticoid excess, making it relevant for studies of hypertension biology and endocrine regulation. 11β-HSD2 is also investigated in placenta and vascular tissues for its role in shaping local glucocorticoid exposure and downstream transcriptional programs.

    11β-HSD2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HSD11B2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HSD11B2. 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 HSD11B2 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 HSD11B2-disrupted clones.

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