α N-catenin Double Nickase Plasmid (h): sc-405168-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α N-catenin 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
- α N-catenin Double Nickase Plasmid (h) and α N-catenin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CTNNA2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α N-catenin Double Nickase Plasmid (h) | sc-405168-NIC | 20 µg | $410.00 | |||
α N-catenin Double Nickase Plasmid (h2) | sc-405168-NIC-2 | 20 µg | $410.00 |
CTNNA2 encodes human α N-catenin, an actin-binding adherens junction protein that links cadherin–β-catenin complexes to the cortical cytoskeleton to stabilize cell–cell adhesion and regulate tissue architecture. By coordinating junctional mechanics, α N-catenin influences cytoskeletal remodeling, neuronal connectivity, and signaling outputs that intersect with Wnt/β-catenin–associated adhesion dynamics. CTNNA2 activity is closely tied to processes such as cell migration and synapse organization, where altered adhesion scaffolding can perturb network formation and cell positioning. Genetic and expression perturbations in CTNNA2 have been associated with neurodevelopmental and neuropsychiatric phenotypes, supporting its utility as a target for mechanistic studies of adhesion-dependent cellular function.
α N-catenin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CTNNA2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CTNNA2. 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 CTNNA2 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 CTNNA2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.