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.
E-cadherin Double Nickase Plasmid (h): sc-400031-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- E-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
- E-cadherin Double Nickase Plasmid (h) and E-cadherin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDH1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: E-cadherin Antibody (G-10): sc-8426
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
E-cadherin Double Nickase Plasmid (h) | sc-400031-NIC | 20 µg | $410.00 | |||
E-cadherin Double Nickase Plasmid (h2) | sc-400031-NIC-2 | 20 µg | $410.00 |
CDH1 encodes E-cadherin, a Ca2+-dependent adherens junction protein that mediates homophilic cell–cell adhesion and maintains epithelial polarity and tissue architecture. Through linkage to β-catenin, p120-catenin, and the actin cytoskeleton, E-cadherin coordinates junctional remodeling, contact inhibition, and mechanotransduction, and it indirectly modulates Wnt/β-catenin signaling by influencing β-catenin availability. Disruption of CDH1 perturbs epithelial barrier integrity and promotes cellular dedifferentiation programs such as epithelial–mesenchymal transition, processes frequently studied in invasion, metastasis-associated phenotypes, and altered tissue morphogenesis. CDH1 loss or dysfunction is recurrent in epithelial cancers and is also implicated in hereditary diffuse gastric cancer, making it a key locus for investigating adhesion-dependent signaling and epithelial homeostasis in human models.
E-cadherin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDH1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDH1. 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 CDH1 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 CDH1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.