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.
CFTR Double Nickase Plasmid (h): sc-400653-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CFTR 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
- CFTR Double Nickase Plasmid (h) and CFTR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CFTR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CFTR Antibody (A-3): sc-376683
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CFTR Double Nickase Plasmid (h) | sc-400653-NIC | 20 µg | $410.00 | |||
CFTR Double Nickase Plasmid (h2) | sc-400653-NIC-2 | 20 µg | $410.00 |
CFTR encodes the cystic fibrosis transmembrane conductance regulator, a cAMP/PKA-regulated ATP-binding cassette ion channel that conducts chloride and bicarbonate across epithelial membranes. CFTR activity coordinates transepithelial fluid secretion, airway surface hydration, and mucociliary clearance, and interfaces with ion transport networks involving ENaC and SLC26 exchangers to maintain epithelial electrolyte balance. Disruption of CFTR-dependent transport alters epithelial homeostasis and inflammatory signaling in tissues such as airway, pancreas, and intestine. Genetic variation in CFTR is strongly linked to cystic fibrosis and contributes to broader CFTR-related disorders, making it a central target for mechanistic studies of epithelial physiology and channel regulation.
CFTR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CFTR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CFTR. 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 CFTR 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 CFTR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.