FPR2 Double Nickase Plasmid (h): sc-401738-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FPR2 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
- FPR2 Double Nickase Plasmid (h) and FPR2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FPR2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: FPR2 Antibody (GM1D6): sc-57141
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FPR2 Double Nickase Plasmid (h) | sc-401738-NIC | 20 µg | $410.00 | |||
FPR2 Double Nickase Plasmid (h2) | sc-401738-NIC-2 | 20 µg | $410.00 |
Formyl peptide receptor 2 (FPR2) is a human G protein–coupled receptor that detects N-formylated peptides and diverse lipid mediators, linking extracellular chemoattractant cues to intracellular signaling. Upon activation it engages Gi-dependent pathways that regulate calcium mobilization, MAPK cascades, PI3K signaling, and β-arrestin–associated processes, shaping leukocyte chemotaxis, degranulation, cytokine output, and phagocyte activation. FPR2 participates in innate immune surveillance and the resolution of inflammation through ligand-biased signaling, integrating pro-inflammatory and pro-resolving programs. Dysregulated FPR2 signaling has been implicated in chronic inflammatory conditions, infection-related immune responses, and tumor-associated inflammation, making it a useful node for dissecting myeloid cell behavior and inflammatory pathway crosstalk.
FPR2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FPR2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FPR2. 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 FPR2 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 FPR2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.