IL-17RA Double Nickase Plasmid (h): sc-401447-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-17RA Double Nickase Plasmid (h) 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-17RA Double Nickase Plasmid (h) and IL-17RA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IL17RA. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-17RA Double Nickase Plasmid (h) | sc-401447-NIC | 20 µg | $410.00 | |||
IL-17RA Double Nickase Plasmid (h2) | sc-401447-NIC-2 | 20 µg | $410.00 |
IL17RA encodes interleukin-17 receptor A (IL-17RA), a widely expressed receptor subunit that forms signaling complexes for IL-17 family cytokines, most prominently IL-17A and IL-17F. Ligand engagement activates adaptor-mediated cascades involving ACT1, TRAF proteins, and downstream NF-κB and MAPK pathways, promoting transcription of chemokines, cytokines, and antimicrobial effectors that coordinate neutrophil recruitment and epithelial barrier responses. IL-17RA-dependent signaling contributes to inflammatory circuit amplification at mucosal surfaces and in stromal and myeloid compartments. Dysregulated IL-17RA activity has been implicated in chronic inflammatory and autoimmune pathobiology, including psoriasis-like inflammation, inflammatory bowel disease-associated pathways, and airway inflammation, as well as tumor-associated inflammation in the microenvironment.
IL-17RA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IL17RA locus in human 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.