Date published: 2026-8-28

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BLVRB Double Nickase Plasmid (m): sc-433230-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • BLVRB 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
  • BLVRB Double Nickase Plasmid (m) and BLVRB Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Blvrb. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BLVRB Antibody (B-9): sc-373692
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    BLVRB Double Nickase Plasmid (m)

    sc-433230-NIC
    20 µg
    $410.00

    Mouse Blvrb encodes biliverdin reductase B (BLVRB), an NAD(P)H-dependent oxidoreductase that catalyzes conversion of biliverdin to bilirubin and contributes to cellular heme catabolism and redox homeostasis. BLVRB activity intersects with oxidative stress responses by modulating intracellular tetrapyrrole pools and influencing reactive oxygen species buffering in erythroid and other metabolically active cells. In addition to roles in iron/heme handling and antioxidant biology, altered biliverdin–bilirubin metabolism has been associated with inflammatory signaling contexts and susceptibility to oxidative damage. Blvrb is therefore a useful target for dissecting how heme turnover and redox enzymes shape cellular stress pathways and phenotype.

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

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