FREM2 Double Nickase Plasmid (h): sc-408000-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FREM2 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
- FREM2 Double Nickase Plasmid (h) and FREM2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FREM2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FREM2 Antibody (F-1): sc-376555
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FREM2 Double Nickase Plasmid (h) | sc-408000-NIC | 20 µg | $410.00 |
FREM2 encodes FRAS1-related extracellular matrix protein 2, a large basement membrane–associated protein that helps organize epithelial–mesenchymal adhesion and stabilize the extracellular matrix during development. FREM2 participates in the FRAS/FREM complex at the epidermal basement membrane, supporting tissue morphogenesis and barrier integrity through regulation of cell–matrix interactions. Disruption of FREM2 has been linked to congenital malformation syndromes, reflecting its role in craniofacial, renal, and limb development. In cell-based models, FREM2 perturbation can alter basement membrane assembly, epithelial polarity, and adhesion-dependent signaling programs.
FREM2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FREM2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FREM2. 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 FREM2 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 FREM2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.