Date published: 2026-8-4

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ADM Double Nickase Plasmid (h): sc-402779-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ADM 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
  • ADM Double Nickase Plasmid (h) and ADM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADM. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ADM Antibody (HTA171/E8): sc-53153
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ADM Double Nickase Plasmid (h)

    sc-402779-NIC
    20 µg
    $410.00

    ADM Double Nickase Plasmid (h2)

    sc-402779-NIC-2
    20 µg
    $410.00

    Adrenomedullin (ADM) is a secreted peptide hormone processed from a larger preproprotein and widely expressed in vascular and endocrine tissues. Through signaling via the calcitonin receptor-like receptor (CALCRL) in complex with RAMP2 or RAMP3, ADM activates cAMP/PKA and downstream MAPK- and PI3K-linked pathways that regulate vasodilation, endothelial barrier function, angiogenic responses, and cellular stress adaptation. ADM is induced by hypoxia and inflammatory cues and contributes to vascular remodeling, fluid homeostasis, and immune–stromal communication. Dysregulated ADM signaling has been associated with cardiometabolic dysfunction, inflammatory states, and tumor-associated angiogenesis, supporting its utility as a mechanistic node in microenvironment and vascular biology research.

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

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