CYP4F3 Double Nickase Plasmid (h): sc-410873-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CYP4F3 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
- CYP4F3 Double Nickase Plasmid (h) and CYP4F3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CYP4F3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYP4F3 Double Nickase Plasmid (h) | sc-410873-NIC | 20 µg | $410.00 | |||
CYP4F3 Double Nickase Plasmid (h2) | sc-410873-NIC-2 | 20 µg | $410.00 |
CYP4F3 encodes a cytochrome P450 ω-hydroxylase that catalyzes the oxidative inactivation of lipid mediators, including leukotriene B4 and related eicosanoids. Through control of these substrates, CYP4F3 contributes to regulation of inflammatory signaling, neutrophil chemotaxis, and resolution pathways linked to arachidonic acid metabolism. The enzyme is also implicated in fatty acid oxidation and redox homeostasis within the endoplasmic reticulum P450 system. Altered CYP4F3 activity or expression has been associated with dysregulated eicosanoid turnover observed in inflammatory conditions and with variation in drug and xenobiotic metabolism phenotypes relevant to pharmacology research.
CYP4F3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CYP4F3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CYP4F3. 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 CYP4F3 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 CYP4F3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.