CLC-KA Double Nickase Plasmid (h): sc-404050-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLC-KA 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
- CLC-KA Double Nickase Plasmid (h) and CLC-KA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CLCNKA. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLC-KA Double Nickase Plasmid (h) | sc-404050-NIC | 20 µg | $410.00 | |||
CLC-KA Double Nickase Plasmid (h2) | sc-404050-NIC-2 | 20 µg | $410.00 |
CLCNKA encodes the kidney-specific chloride channel CLC-KA, a member of the CLC family that conducts Cl⁻ across epithelial membranes and supports transepithelial salt reabsorption. CLC-KA activity contributes to electrolyte and water homeostasis in the nephron by coupling with transport processes that shape tubular ion gradients and influence fluid balance. Altered CLCNKA function is linked to inherited salt-wasting tubulopathies and blood pressure–related phenotypes, making it relevant for studies of renal ion handling and transport physiology. The gene is commonly investigated in cellular models of nephron epithelia to interrogate chloride conductance, channel regulation, and compensatory remodeling of solute transport networks.
CLC-KA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CLCNKA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CLCNKA. 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 CLCNKA 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 CLCNKA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.