Cytokeratin 6B Double Nickase Plasmid (h): sc-401651-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cytokeratin 6B 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 6B Double Nickase Plasmid (h) and Cytokeratin 6B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KRT6B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cytokeratin 6B Double Nickase Plasmid (h) | sc-401651-NIC | 20 µg | $410.00 | |||
Cytokeratin 6B Double Nickase Plasmid (h2) | sc-401651-NIC-2 | 20 µg | $410.00 |
KRT6B encodes cytokeratin 6B, a type II intermediate filament protein that heterodimerizes with type I keratins to form the cytoskeletal network of stratified epithelia. Cytokeratin 6B contributes to mechanical stability, epithelial differentiation, and stress-induced remodeling, coordinating with desmosomal and hemidesmosomal adhesion complexes to maintain tissue integrity. Its expression is tightly linked to wound repair programs and keratinocyte activation states, intersecting with pathways governing cytoskeletal organization, cell migration, and barrier function. Dysregulated keratin 6B expression or keratin network perturbation is associated with epithelial hyperproliferation and genodermatoses phenotypes, supporting its use as a marker and functional node in skin biology and keratinization research.
Cytokeratin 6B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KRT6B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KRT6B. 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 KRT6B 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 KRT6B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.