COL17A1 Double Nickase Plasmid (h): sc-402747-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- COL17A1 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
- COL17A1 Double Nickase Plasmid (h) and COL17A1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting COL17A1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
COL17A1 Double Nickase Plasmid (h) | sc-402747-NIC | 20 µg | $410.00 | |||
COL17A1 Double Nickase Plasmid (h2) | sc-402747-NIC-2 | 20 µg | $410.00 |
COL17A1 encodes collagen type XVII alpha 1, a transmembrane component of hemidesmosomes that anchors basal keratinocytes to the basement membrane through interactions with laminin-332 and integrins. By stabilizing dermal–epidermal adhesion and organizing extracellular matrix contacts, COL17A1 supports epidermal integrity, mechanical resilience, and epithelial homeostasis. Altered COL17A1 expression or function is linked to skin blistering phenotypes and autoimmune targeting at the dermal–epidermal junction, and it is also studied in the context of epithelial remodeling and tumor invasion. These properties make COL17A1 a useful target for investigating adhesion signaling, matrix–cell interfaces, and junctional stability in human epithelial systems.
COL17A1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the COL17A1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within COL17A1. 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 COL17A1 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 COL17A1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.