IFN-α/βRα Double Nickase Plasmid (m): sc-421047-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-α/βRα Double Nickase Plasmid (m) 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
- IFN-α/βRα Double Nickase Plasmid (m) and IFN-α/βRα Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ifnar1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IFN-α/βRα Antibody (E-12): sc-393089
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-α/βRα Double Nickase Plasmid (m) | sc-421047-NIC | 20 µg | $410.00 | |||
IFN-α/βRα Double Nickase Plasmid (m2) | sc-421047-NIC-2 | 20 µg | $410.00 |
Mouse Ifnar1 encodes interferon alpha/beta receptor alpha (IFN-α/βRα), a core subunit of the type I interferon receptor complex that initiates antiviral and immunomodulatory signaling upon IFN-α/β binding. Receptor engagement activates JAK1 and TYK2, driving STAT1/STAT2 phosphorylation, ISGF3 assembly with IRF9, and transcription of interferon-stimulated genes that regulate innate immune activation, antigen presentation, and cell survival. IFNAR1 signaling also intersects with NF-κB and MAPK pathways to shape inflammatory outputs and crosstalk with pattern-recognition receptor responses. Dysregulated IFNAR1-dependent programs are frequently studied in contexts of viral susceptibility, chronic inflammation, and autoimmunity-associated immune dysregulation, as well as tumor-immune interactions.
IFN-α/βRα Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ifnar1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ifnar1. 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 Ifnar1 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 Ifnar1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.