FLAP Double Nickase Plasmid (h): sc-402268-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FLAP 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
- FLAP Double Nickase Plasmid (h) and FLAP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ALOX5AP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FLAP Double Nickase Plasmid (h) | sc-402268-NIC | 20 µg | $410.00 | |||
FLAP Double Nickase Plasmid (h2) | sc-402268-NIC-2 | 20 µg | $410.00 |
Human ALOX5AP encodes 5-lipoxygenase-activating protein (FLAP), an integral nuclear membrane protein that facilitates arachidonic acid delivery to 5-lipoxygenase to support leukotriene biosynthesis. FLAP functions within the eicosanoid metabolism network, shaping lipid mediator profiles that influence leukocyte chemotaxis, vascular tone, and inflammatory signaling. Through regulation of leukotriene production, ALOX5AP links innate immune activation to downstream GPCR- and cytokine-driven pathways that modulate cellular recruitment and tissue responses. Altered FLAP activity or expression has been associated with dysregulated inflammatory phenotypes and cardiometabolic and neuroinflammatory disease contexts, making it a relevant target for mechanistic studies in myeloid and vascular cell models.
FLAP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ALOX5AP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ALOX5AP. 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 ALOX5AP 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 ALOX5AP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.