T2-cadherin Double Nickase Plasmid (h): sc-401926-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- T2-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
- T2-cadherin Double Nickase Plasmid (h) and T2-cadherin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDH10. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T2-cadherin Double Nickase Plasmid (h) | sc-401926-NIC | 20 µg | $410.00 | |||
T2-cadherin Double Nickase Plasmid (h2) | sc-401926-NIC-2 | 20 µg | $410.00 |
CDH10 encodes T2-cadherin, a calcium-dependent cell–cell adhesion molecule of the cadherin superfamily that contributes to tissue patterning and maintenance of epithelial and neuronal architecture. Through homophilic adhesion and linkage to catenin-associated complexes, T2-cadherin influences cytoskeletal organization, contact-dependent signaling, and cellular migration programs. CDH10 expression and sequence variation have been associated with neurodevelopmental phenotypes and altered circuit connectivity, and dysregulation of cadherin-mediated adhesion is broadly relevant to oncogenic processes such as invasion and metastasis. As a result, CDH10 is frequently studied in models of cell adhesion, morphogenesis, synaptic connectivity, and context-dependent changes in differentiation and motility.
T2-cadherin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDH10 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDH10. 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 CDH10 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 CDH10-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.