IRAK-4 Double Nickase Plasmid (m): sc-435222-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IRAK-4 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
- IRAK-4 Double Nickase Plasmid (m) and IRAK-4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Irak4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IRAK-4 Double Nickase Plasmid (m) | sc-435222-NIC | 20 µg | $410.00 | |||
IRAK-4 Double Nickase Plasmid (m2) | sc-435222-NIC-2 | 20 µg | $410.00 |
Irak4 encodes interleukin-1 receptor–associated kinase 4 (IRAK-4), a serine/threonine kinase that functions as an essential proximal signaling node downstream of MyD88-dependent Toll-like receptor and IL-1 receptor complexes in mouse innate immune cells. Upon receptor engagement, IRAK-4 promotes assembly of the myddosome and phosphorylation events that propagate signaling to TRAF6, culminating in activation of NF-κB and MAPK pathways and induction of inflammatory gene programs. This axis regulates cytokine production, leukocyte activation, and antimicrobial responses, and is widely studied in the context of dysregulated inflammation and immune signaling phenotypes. IRAK-4 is therefore a key molecular entry point for dissecting pattern-recognition receptor signaling and inflammatory transcriptional control in cellular and in vivo models.
IRAK-4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Irak4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Irak4. 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 Irak4 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 Irak4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.