Notum Double Nickase Plasmid (m): sc-429545-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Notum 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
- Notum Double Nickase Plasmid (m) and Notum Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Notum. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Notum Double Nickase Plasmid (m) | sc-429545-NIC | 20 µg | $410.00 |
Mouse Notum encodes a secreted carboxylesterase that deacylates Wnt ligands, thereby antagonizing canonical Wnt/β-catenin signaling and modulating tissue patterning and stem cell–associated transcriptional programs. By limiting Wnt receptor engagement through removal of the palmitoleate modification, Notum contributes to extracellular feedback control of morphogen gradients and influences cell fate decisions during development and adult tissue homeostasis. Altered NOTUM activity has been linked to dysregulated Wnt pathway output in contexts such as bone remodeling, metabolic regulation, and tumor biology, making it a useful node for mechanistic studies of Wnt-dependent processes. In mouse models, Notum perturbation supports investigation of pathway crosstalk affecting proliferation, differentiation, and niche signaling.
Notum Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Notum locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Notum. 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 Notum 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 Notum-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.