IL-17RE Double Nickase Plasmid (h): sc-405190-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-17RE 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-17RE Double Nickase Plasmid (h) and IL-17RE Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IL17RE. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-17RE Double Nickase Plasmid (h) | sc-405190-NIC | 20 µg | $410.00 | |||
IL-17RE Double Nickase Plasmid (h2) | sc-405190-NIC-2 | 20 µg | $410.00 |
IL17RE encodes IL‑17RE, a type I transmembrane receptor subunit that binds IL‑17C and cooperates with IL‑17RA to initiate IL‑17 family signaling. Ligand engagement promotes recruitment of the adaptor ACT1 (TRAF3IP2) and downstream TRAF-dependent cascades that activate NF‑κB, MAPK, and C/EBP transcriptional programs, driving epithelial and mucosal inflammatory gene expression. IL‑17RE is highly relevant to barrier tissue biology, shaping antimicrobial responses and chemokine production that regulate neutrophil and myeloid cell trafficking. Dysregulated IL‑17C/IL‑17RE signaling has been implicated in chronic inflammatory conditions, including inflammatory bowel disease and psoriasis-like skin inflammation, and is studied in the context of tumor-associated inflammation in epithelial cancers.
IL-17RE Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IL17RE locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IL17RE. 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 IL17RE 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 IL17RE-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.