T1-cadherin Double Nickase Plasmid (h): sc-401986-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- T1-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
- T1-cadherin Double Nickase Plasmid (h) and T1-cadherin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDH9. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T1-cadherin Double Nickase Plasmid (h) | sc-401986-NIC | 20 µg | $410.00 | |||
T1-cadherin Double Nickase Plasmid (h2) | sc-401986-NIC-2 | 20 µg | $410.00 |
CDH9 encodes T1-cadherin, a classical cadherin-family cell adhesion molecule that contributes to calcium-dependent homophilic interactions and tissue-specific cell–cell recognition. Through coupling to cytoskeletal organization and contact-dependent signaling, CDH9 can influence cell sorting, neurite targeting, and maintenance of differentiated cellular architecture. Altered cadherin-mediated adhesion and associated junctional remodeling are recurrent features of disease-relevant processes, including dysregulated migration and aberrant connectivity. As a result, CDH9 is frequently studied in models linking adhesion dynamics to developmental phenotypes and pathologic changes in tissue organization.
T1-cadherin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDH9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDH9. 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 CDH9 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 CDH9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.