Date published: 2026-7-4

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BMP-3 Double Nickase Plasmid (h): sc-404417-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • BMP-3 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
  • BMP-3 Double Nickase Plasmid (h) and BMP-3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BMP3. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    BMP-3 Double Nickase Plasmid (h)

    sc-404417-NIC
    20 µg
    $410.00

    BMP-3 Double Nickase Plasmid (h2)

    sc-404417-NIC-2
    20 µg
    $410.00

    Human BMP3 encodes bone morphogenetic protein 3 (BMP-3), a secreted TGF-β superfamily ligand that modulates cell fate decisions in skeletal and connective tissues. BMP-3 generally acts as an antagonist of osteogenic BMP signaling, influencing SMAD-mediated transcriptional programs that regulate osteoblast differentiation, bone remodeling, and extracellular matrix homeostasis. Through crosstalk with BMP/SMAD and related developmental pathways, BMP-3 contributes to tissue patterning and skeletal morphogenesis. Dysregulated BMP3 expression or signaling balance has been associated with altered bone density and remodeling phenotypes and has been examined in contexts where TGF-β family signaling is perturbed, including fibrosis and cancer biology.

    BMP-3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BMP3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BMP3. 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 BMP3 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 BMP3-disrupted clones.

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