IFN-α/βRβ Double Nickase Plasmid (m): sc-421048-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-α/βRβ 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/βRβ Double Nickase Plasmid (m) and IFN-α/βRβ Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ifnar2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IFN-α/βRβ Antibody (F-7): sc-137209
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-α/βRβ Double Nickase Plasmid (m) | sc-421048-NIC | 20 µg | $410.00 |
Ifnar2 encodes interferon alpha/beta receptor beta (IFN-α/βRβ), a core subunit of the type I interferon receptor complex required for cellular responses to IFN-α and IFN-β. Ligand engagement initiates JAK1/TYK2-dependent phosphorylation cascades that activate STAT1/STAT2 and IRF9 to form ISGF3, driving transcription of interferon-stimulated genes that regulate antiviral restriction, antigen presentation, and innate immune programming. IFNAR2 signaling intersects with NF-κB and MAPK pathways to shape cytokine production and immune cell differentiation. Dysregulated type I interferon signaling is implicated in inflammatory and autoimmune phenotypes and influences tumor–immune interactions, making Ifnar2 a common target for mechanistic studies of immune signaling networks.
IFN-α/βRβ Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ifnar2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ifnar2. 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 Ifnar2 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 Ifnar2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.