IL-1ra Double Nickase Plasmid (m): sc-421102-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-1ra 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
- IL-1ra Double Nickase Plasmid (m) and IL-1ra Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Il1rn. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-1ra Double Nickase Plasmid (m) | sc-421102-NIC | 20 µg | $410.00 | |||
IL-1ra Double Nickase Plasmid (m2) | sc-421102-NIC-2 | 20 µg | $410.00 |
Mouse Il1rn encodes IL-1 receptor antagonist (IL-1ra), an endogenous competitive inhibitor of IL-1α/IL-1β signaling that limits activation of IL-1R1 and downstream MyD88-dependent NF-κB and MAPK pathways. By restraining pro-inflammatory transcriptional programs and cytokine amplification, IL-1ra contributes to regulation of innate immune cell activation, leukocyte recruitment, and tissue homeostasis. Altered Il1rn activity is used to model dysregulated inflammation, including arthritis-like phenotypes, inflammatory bowel pathology, and skin inflammation, providing a tractable axis for studying cytokine network feedback and resolution mechanisms.
IL-1ra Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Il1rn locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Il1rn. 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 Il1rn 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 Il1rn-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.