FAS Double Nickase Plasmid (m): sc-420287-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FAS Double Nickase Plasmid (m) 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 (m) and FAS Double Nickase Plasmid (m2) 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 (C236): sc-21730
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAS Double Nickase Plasmid (m) | sc-420287-NIC | 20 µg | $410.00 | |||
FAS Double Nickase Plasmid (m2) | sc-420287-NIC-2 | 20 µg | $410.00 |
Fas encodes the FAS (CD95/TNFRSF6) death receptor, a key initiator of extrinsic apoptosis following engagement by FAS ligand and assembly of the death-inducing signaling complex. Receptor activation recruits FADD and promotes caspase-8 activation, linking to downstream effector caspases and, in some contexts, mitochondrial amplification via BID cleavage. Beyond apoptosis, FAS signaling can intersect with NF-κB and MAPK pathways to influence immune homeostasis, peripheral tolerance, and inflammation. Dysregulated FAS activity is implicated in defective lymphocyte deletion, autoimmune phenotypes, and altered susceptibility to tumor immune evasion, making mouse Fas a widely used node for mechanistic studies in immunology and cell death.
FAS Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Fas locus in mouse 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.