Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
beta-catenin Double Nickase Plasmid (m): sc-419477-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- beta-catenin 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
- beta-catenin Double Nickase Plasmid (m) and beta-catenin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ctnnb1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: beta-catenin Antibody (E-5): sc-7963
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
beta-catenin Double Nickase Plasmid (m) | sc-419477-NIC | 20 µg | $410.00 | |||
beta-catenin Double Nickase Plasmid (m2) | sc-419477-NIC-2 | 20 µg | $410.00 |
Mouse Ctnnb1 encodes beta-catenin, a multifunctional armadillo-repeat protein that couples cadherin-based adherens junctions to the actin cytoskeleton and regulates cell–cell adhesion and tissue architecture. In canonical Wnt signaling, stabilized beta-catenin accumulates in the cytoplasm and translocates to the nucleus to partner with TCF/LEF transcription factors, coordinating programs that control proliferation, differentiation, and stem cell maintenance. Beta-catenin activity is modulated by the destruction complex (including APC, AXIN, and GSK3), integrating inputs from developmental cues and stress-responsive pathways. Dysregulation of beta-catenin signaling or adhesion functions is implicated in oncogenic transformation, developmental defects, and inflammatory pathologies, making Ctnnb1 a central node for mechanistic studies.
beta-catenin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ctnnb1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ctnnb1. 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 Ctnnb1 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 Ctnnb1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.