FPR Double Nickase Plasmid (h): sc-418173-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FPR 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
- FPR Double Nickase Plasmid (h) and FPR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FPR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FPR Double Nickase Plasmid (h) | sc-418173-NIC | 20 µg | $410.00 | |||
FPR Double Nickase Plasmid (h2) | sc-418173-NIC-2 | 20 µg | $410.00 |
Formyl peptide receptor 1 (FPR1) encodes FPR, a Gi-coupled GPCR that detects N-formylated peptides and other chemotactic ligands to guide neutrophil and monocyte migration. Ligand binding activates PLCβ/Ca²⁺ flux, PI3K–AKT, MAPK, and small GTPase signaling, coordinating actin remodeling, degranulation, and NADPH oxidase-dependent reactive oxygen species production during innate immune responses. FPR1 activity shapes leukocyte trafficking and inflammatory mediator release, linking it to dysregulated inflammation and tissue injury contexts. Altered FPR1 signaling has been studied in infectious and sterile inflammatory settings, and in the tumor microenvironment where myeloid chemotaxis can influence immune composition.
FPR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FPR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FPR1. 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 FPR1 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 FPR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.