FADS1 Double Nickase Plasmid (h): sc-404735-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FADS1 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
- FADS1 Double Nickase Plasmid (h) and FADS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FADS1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FADS1 Antibody (7-RY13): sc-134337
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FADS1 Double Nickase Plasmid (h) | sc-404735-NIC | 20 µg | $410.00 | |||
FADS1 Double Nickase Plasmid (h2) | sc-404735-NIC-2 | 20 µg | $410.00 |
FADS1 encodes fatty acid desaturase 1, a Δ5-desaturase that catalyzes a key rate-limiting step in the biosynthesis of long-chain polyunsaturated fatty acids by converting dihomo-γ-linolenic acid to arachidonic acid and related substrates to downstream eicosanoid precursors. Through regulation of membrane lipid composition and lipid mediator availability, FADS1 influences inflammatory signaling, metabolic homeostasis, and cell signaling processes linked to phospholipid remodeling and arachidonic acid metabolism. Genetic variation and altered expression of FADS1 have been associated with shifts in circulating lipid profiles and susceptibility to complex traits involving cardiometabolic and inflammatory phenotypes, making it a relevant target for mechanistic studies of lipid-driven cellular programs. In human cell models, perturbing FADS1 supports investigation of metabolic flux, membrane dynamics, and lipid mediator–dependent transcriptional responses.
FADS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FADS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FADS1. 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 FADS1 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 FADS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.