Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
IL-17R Double Nickase Plasmid (m): sc-421093-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-17R 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-17R Double Nickase Plasmid (m) and IL-17R Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Il17ra. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IL-17R Antibody (G-9): sc-376374
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-17R Double Nickase Plasmid (m) | sc-421093-NIC | 20 µg | $410.00 | |||
IL-17R Double Nickase Plasmid (m2) | sc-421093-NIC-2 | 20 µg | $410.00 |
Mouse Il17ra encodes IL-17R, a type I transmembrane receptor subunit that binds IL-17 family cytokines to initiate pro-inflammatory signaling in epithelial and stromal compartments as well as myeloid lineages. Ligand engagement promotes recruitment of the adaptor ACT1 and activation of downstream NF-κB, MAPK, and C/EBP pathways, driving chemokine and cytokine programs that coordinate neutrophil mobilization and barrier immunity. IL-17R signaling intersects with Th17-driven immune responses and contributes to tissue inflammation and remodeling in models of autoimmune and inflammatory disease, including arthritis, dermatitis, and airway inflammation. Dissecting Il17ra function is therefore important for studying cytokine-driven host defense mechanisms and inflammatory network regulation in mouse systems.
IL-17R Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Il17ra locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Il17ra. 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 Il17ra 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 Il17ra-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.