IRF3 Double Nickase Plasmid (m): sc-424792-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IRF3 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
- IRF3 Double Nickase Plasmid (m) and IRF3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Irf3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IRF3 Antibody (D-3): sc-376455
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IRF3 Double Nickase Plasmid (m) | sc-424792-NIC | 20 µg | $410.00 |
Mouse Irf3 encodes interferon regulatory factor 3 (IRF3), a central transcription factor in innate antiviral immunity that couples cytosolic nucleic acid sensing to type I interferon and interferon-stimulated gene expression. Following activation downstream of PRR pathways including cGAS–STING, RIG-I/MDA5–MAVS, and TLR3–TRIF, IRF3 is phosphorylated by TBK1/IKKε, dimerizes, and translocates to the nucleus to coordinate inflammatory and antiviral transcriptional programs. IRF3 signaling intersects with NF-κB and IRF7 to shape cytokine output, apoptosis, and immunometabolic remodeling during infection and sterile inflammation. Dysregulated IRF3 activity has been implicated in susceptibility to viral infection, aberrant interferon responses, and inflammatory pathologies, making Irf3 a key node for mechanistic studies of innate immune signaling.
IRF3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Irf3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Irf3. 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 Irf3 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 Irf3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.