Date published: 2026-7-7

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RANK Double Nickase Plasmid (m): sc-423439-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • RANK 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
  • RANK Double Nickase Plasmid (m) and RANK Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tnfrsf11a. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RANK Antibody (H-7): sc-374360
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    RANK Double Nickase Plasmid (m)

    sc-423439-NIC
    20 µg
    $410.00

    Mouse Tnfrsf11a encodes RANK (receptor activator of NF-κB), a TNF receptor superfamily member that transduces RANKL-dependent signals to regulate osteoclast differentiation, bone remodeling, and immune cell communication. Upon ligand binding, RANK recruits adaptor proteins such as TRAFs to activate NF-κB, MAPK, and AP-1 pathways, coordinating survival and differentiation programs in myeloid lineages. RANK signaling is tightly linked to osteoimmunology, with dysregulation influencing inflammatory bone loss and altered hematopoietic microenvironments. These functions make Tnfrsf11a a key target for dissecting coupling between immune signaling and skeletal turnover in mouse models.

    RANK Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tnfrsf11a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tnfrsf11a. 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 Tnfrsf11a 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 Tnfrsf11a-disrupted clones.

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