Date published: 2026-7-11

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OSX Double Nickase Plasmid (m): sc-431270-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • OSX 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
  • OSX Double Nickase Plasmid (m) and OSX Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sp7. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: OSX Antibody (F-3): sc-393325
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    OSX Double Nickase Plasmid (m)

    sc-431270-NIC
    20 µg
    $410.00

    OSX Double Nickase Plasmid (m2)

    sc-431270-NIC-2
    20 µg
    $410.00

    Mouse Sp7 encodes osterix (OSX), a zinc-finger transcription factor that is essential for osteoblast lineage commitment and maturation downstream of BMP and Wnt/β-catenin signaling. OSX coordinates transcriptional programs controlling extracellular matrix deposition and mineralization, including regulation of genes such as Bglap, Col1a1, and Alpl. In bone development and remodeling, Sp7 activity integrates cues from osteogenic progenitors to drive differentiation while modulating interactions with RUNX2-dependent pathways. Dysregulated Sp7/OSX function is linked to impaired ossification and skeletal phenotypes, making it relevant for studies of bone biology, fracture repair, and osteogenesis-related disorders.

    OSX Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sp7 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sp7. 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 Sp7 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 Sp7-disrupted clones.

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