FRAS1 Double Nickase Plasmid (h): sc-407225-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FRAS1 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
- FRAS1 Double Nickase Plasmid (h) and FRAS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FRAS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FRAS1 Double Nickase Plasmid (h) | sc-407225-NIC | 20 µg | $410.00 |
FRAS1 encodes an extracellular matrix–associated protein that localizes to basement membrane zones and supports epithelial–mesenchymal adhesion during embryonic morphogenesis. It participates in anchoring and stabilization of epithelial structures, influencing processes such as skin integrity, craniofacial development, and renal morphogenesis through cell–matrix interactions. Disruption of FRAS1 is linked to Fraser syndrome spectrum phenotypes and congenital anomalies, highlighting its importance in developmental pathways governing tissue organization. As a large matrix protein, FRAS1 is frequently studied in the context of basement membrane assembly, epithelial barrier formation, and mechanisms underlying developmental malformations.
FRAS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FRAS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FRAS1. 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 FRAS1 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 FRAS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.