BR-cadherin Double Nickase Plasmid (h): sc-401987-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BR-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
- BR-cadherin Double Nickase Plasmid (h) and BR-cadherin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDH12. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BR-cadherin Double Nickase Plasmid (h) | sc-401987-NIC | 20 µg | $410.00 | |||
BR-cadherin Double Nickase Plasmid (h2) | sc-401987-NIC-2 | 20 µg | $410.00 |
CDH12 encodes BR-cadherin, a calcium-dependent cell–cell adhesion molecule of the classical cadherin family that supports tissue architecture through homophilic interactions and coupling to catenins. By linking adherens junctions to the actin cytoskeleton, BR-cadherin influences contact-dependent signaling, cellular polarity, and coordinated migration during development and tissue remodeling. CDH12 expression has been associated with neural and epithelial organization, and dysregulation of cadherin-mediated adhesion is broadly relevant to invasive behavior and altered differentiation programs in disease biology. As a junctional regulator, BR-cadherin provides a tractable entry point for studying how adhesion state rewires intracellular signaling and morphogenetic processes.
BR-cadherin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDH12 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDH12. 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 CDH12 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 CDH12-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.