frizzled-7 Double Nickase Plasmid (m): sc-420437-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- frizzled-7 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
- frizzled-7 Double Nickase Plasmid (m) and frizzled-7 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Fzd7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
frizzled-7 Double Nickase Plasmid (m) | sc-420437-NIC | 20 µg | $410.00 |
Mouse Fzd7 encodes frizzled-7, a seven-transmembrane WNT receptor that coordinates ligand-dependent signaling through canonical β-catenin/TCF transcription and non-canonical planar cell polarity and WNT/Ca²⁺ pathways. By regulating cell fate decisions, proliferation, polarity, and migration, frizzled-7 contributes to embryonic patterning and adult tissue homeostasis, including stem and progenitor cell maintenance. Altered Fzd7-mediated signaling has been linked to dysregulated WNT pathway activity observed in models of oncogenesis, fibrosis, and inflammatory tissue remodeling, where shifts in β-catenin output and cytoskeletal dynamics can influence disease-relevant phenotypes. Accordingly, Fzd7 is widely studied in pathways governing epithelial organization, regenerative responses, and niche-dependent signaling crosstalk.
frizzled-7 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Fzd7 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Fzd7. 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 Fzd7 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 Fzd7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.