vezatin Double Nickase Plasmid (h): sc-418454-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- vezatin 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
- vezatin Double Nickase Plasmid (h) and vezatin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting VEZT. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: vezatin Antibody (B-1): sc-271347
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
vezatin Double Nickase Plasmid (h) | sc-418454-NIC | 20 µg | $410.00 |
VEZT encodes vezatin, a transmembrane component of adherens junctions that couples the cadherin–catenin complex to the actin cytoskeleton and helps stabilize cell–cell adhesion. Vezatin participates in epithelial polarity and tissue architecture by supporting junctional remodeling during morphogenesis and by influencing cytoskeletal dynamics. Disruption of VEZT expression or junctional localization can alter barrier integrity and cell migration programs, processes frequently implicated in epithelial dysplasia and tumor progression. As a junction-associated scaffold, vezatin is also relevant to studying mechanotransduction and signaling crosstalk at the plasma membrane, including pathways that respond to changes in cell adhesion.
vezatin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the VEZT locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within VEZT. 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 VEZT 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 VEZT-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.