Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CD89 Double Nickase Plasmid (h): sc-403014-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD89 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
- CD89 Double Nickase Plasmid (h) and CD89 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FCAR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CD89 Antibody (A3): sc-19680
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD89 Double Nickase Plasmid (h) | sc-403014-NIC | 20 µg | $410.00 | |||
CD89 Double Nickase Plasmid (h2) | sc-403014-NIC-2 | 20 µg | $410.00 |
FCAR encodes CD89 (FcαRI), a myeloid lineage immunoglobulin receptor that binds IgA and couples to the FcR γ-chain to transduce activating or inhibitory signals depending on receptor configuration. CD89 engagement regulates phagocytosis, antibody-dependent cellular cytotoxicity, oxidative burst, cytokine release, and inflammatory gene expression through ITAM-mediated signaling pathways involving Src family kinases, SYK, PI3K, and downstream NF-κB and MAPK cascades. This receptor is prominently expressed on neutrophils, monocytes, macrophages, eosinophils, and certain dendritic cell subsets, shaping mucosal and systemic immune responses to opsonized microbes and immune complexes. Dysregulated IgA–CD89 signaling and altered FCAR expression have been implicated in immune complex–driven inflammation and myeloid cell dysfunction relevant to inflammatory and autoimmune disease biology.
CD89 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FCAR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FCAR. 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 FCAR 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 FCAR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.