frizzled-10 Double Nickase Plasmid (h): sc-406690-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- frizzled-10 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
- frizzled-10 Double Nickase Plasmid (h) and frizzled-10 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FZD10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
frizzled-10 Double Nickase Plasmid (h) | sc-406690-NIC | 20 µg | $410.00 |
FZD10 encodes frizzled-10, a seven-transmembrane Wnt receptor that binds Wnt ligands to regulate β-catenin–dependent transcription as well as non-canonical Wnt/planar cell polarity and Ca2+-linked signaling. Through these pathways, frizzled-10 influences cell fate specification, proliferation, polarity, and migration programs that are central to embryonic development and tissue homeostasis. Dysregulated FZD10/Wnt signaling has been associated with altered differentiation states and oncogenic signaling networks in multiple tumor contexts, and it is also relevant to studies of stem-like phenotypes and epithelial–mesenchymal dynamics. As a surface receptor, frizzled-10 provides a tractable node for dissecting pathway cross-talk between Wnt, growth factor signaling, and cytoskeletal remodeling.
frizzled-10 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FZD10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FZD10. 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 FZD10 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 FZD10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.