Wnt-7b Double Nickase Plasmid (m): sc-423722-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Wnt-7b 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
- Wnt-7b Double Nickase Plasmid (m) and Wnt-7b Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Wnt7b. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Wnt-7b Double Nickase Plasmid (m) | sc-423722-NIC | 20 µg | $410.00 | |||
Wnt-7b Double Nickase Plasmid (m2) | sc-423722-NIC-2 | 20 µg | $410.00 |
Mouse Wnt7b encodes Wnt-7b, a secreted glycoprotein ligand that activates Wnt signaling to regulate embryonic patterning, tissue morphogenesis, and organ-specific cell fate decisions. Wnt-7b can engage Frizzled/LRP receptors to stimulate canonical β-catenin–dependent transcription as well as non-canonical signaling programs that shape proliferation, polarity, and migration. In developmental and tissue homeostasis contexts, Wnt-7b activity has been linked to epithelial–mesenchymal interactions and vascular remodeling, making it relevant for studying dysregulated Wnt pathway outputs observed across diverse disease models. Altered Wnt7b expression or signaling tone is frequently investigated for its impact on differentiation states, extracellular matrix dynamics, and pathway cross-talk with growth factor and inflammatory signaling.
Wnt-7b Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Wnt7b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Wnt7b. 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 Wnt7b 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 Wnt7b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.