Date published: 2026-8-16

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LRP5 Double Nickase Plasmid (m): sc-421465-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • LRP5 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
  • LRP5 Double Nickase Plasmid (m) and LRP5 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lrp5. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LRP5 Antibody (B-9): sc-390267
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    LRP5 Double Nickase Plasmid (m)

    sc-421465-NIC
    20 µg
    $410.00

    Lrp5 encodes low-density lipoprotein receptor-related protein 5 (LRP5), a single-pass co-receptor that potentiates canonical Wnt/β-catenin signaling by forming ligand-induced complexes with Frizzled receptors. In mouse tissues, LRP5 contributes to osteoblast activity, bone mass regulation, and metabolic homeostasis, and it can influence cell proliferation and differentiation programs through β-catenin–dependent transcription. LRP5 also intersects with extracellular modulators such as DKK and sclerostin and coordinates pathway output in development and tissue remodeling. Dysregulated Lrp5 signaling is widely used to model mechanisms relevant to skeletal phenotypes and Wnt-driven changes in tissue physiology.

    LRP5 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lrp5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lrp5. 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 Lrp5 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 Lrp5-disrupted clones.

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