Cytokeratin 6A Double Nickase Plasmid (h): sc-401650-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cytokeratin 6A 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
- Cytokeratin 6A Double Nickase Plasmid (h) and Cytokeratin 6A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KRT6A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cytokeratin 6A Double Nickase Plasmid (h) | sc-401650-NIC | 20 µg | $410.00 | |||
Cytokeratin 6A Double Nickase Plasmid (h2) | sc-401650-NIC-2 | 20 µg | $410.00 |
KRT6A encodes cytokeratin 6A, a type II intermediate filament protein that heterodimerizes with type I keratins to build the keratin cytoskeleton in stratified epithelia. Cytokeratin 6A supports mechanical resilience, regulates keratinocyte migration and wound-associated remodeling, and interfaces with desmosomal adhesion and cytoskeletal signaling pathways that coordinate stress responses. Its expression is induced during hyperproliferation and tissue repair, linking KRT6A to epithelial differentiation programs and barrier maintenance. Dysregulated KRT6A has been associated with keratinization disorders and epithelial pathologies, making it relevant for studies of epidermal biology, cytoskeletal organization, and stress-induced transcriptional networks.
Cytokeratin 6A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KRT6A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KRT6A. 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 KRT6A 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 KRT6A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.