FAS Double Nickase Plasmid (h): sc-400481-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAS 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
- FAS Double Nickase Plasmid (h) and FAS Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FAS. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FAS Antibody (B-10): sc-8009
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAS Double Nickase Plasmid (h) | sc-400481-NIC | 20 µg | $410.00 | |||
FAS Double Nickase Plasmid (h2) | sc-400481-NIC-2 | 20 µg | $410.00 |
FAS (CD95/TNFRSF6) encodes a death receptor that initiates extrinsic apoptosis upon binding Fas ligand, driving DISC assembly with FADD and caspase-8 activation. This signaling axis integrates with mitochondrial amplification via BID and intersects with NF-κB and MAPK pathways to coordinate immune homeostasis, peripheral tolerance, and termination of activated lymphocytes. Perturbation of FAS signaling is linked to defective activation-induced cell death and lymphoproliferation, and altered FAS regulation has been observed across multiple malignancies and inflammatory contexts. As a membrane receptor with strong pathway connectivity, FAS is frequently studied to dissect apoptosis thresholds, immune cell selection, and mechanisms of cell death resistance.
FAS Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FAS locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FAS. 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 FAS 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 FAS-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.