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.
P-cadherin Double Nickase Plasmid (h): sc-400507-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- P-cadherin 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
- P-cadherin Double Nickase Plasmid (h) and P-cadherin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDH3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: P-cadherin Antibody (A-10): sc-74545
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
P-cadherin Double Nickase Plasmid (h) | sc-400507-NIC | 20 µg | $410.00 | |||
P-cadherin Double Nickase Plasmid (h2) | sc-400507-NIC-2 | 20 µg | $410.00 |
CDH3 encodes P-cadherin, a classical calcium-dependent cell–cell adhesion molecule localized to adherens junctions where it links to catenins and the actin cytoskeleton to regulate epithelial cohesion, polarity, and tissue morphogenesis. By modulating junctional stability and contact-dependent signaling, P-cadherin influences pathways governing cell migration, differentiation, and cytoskeletal remodeling, including interactions with WNT/β-catenin and Rho-family GTPase networks. Altered CDH3 expression or junctional organization is associated with disrupted epithelial architecture and has been studied in the context of invasion-related phenotypes and tumor heterogeneity. CDH3 is also implicated in developmental and inherited epithelial disorders, making it relevant for mechanistic studies of adhesion-driven signaling and barrier function.
P-cadherin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDH3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDH3. 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 CDH3 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 CDH3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.