IL-28R Double Nickase Plasmid (h): sc-402530-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-28R 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-28R Double Nickase Plasmid (h) and IL-28R Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IFNLR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-28R Double Nickase Plasmid (h) | sc-402530-NIC | 20 µg | $410.00 | |||
IL-28R Double Nickase Plasmid (h2) | sc-402530-NIC-2 | 20 µg | $410.00 |
IFNLR1 encodes interferon lambda receptor 1 (IL-28R), the ligand-binding subunit of the type III interferon receptor complex that pairs with IL10RB to mediate responses to IFN-λ cytokines. Upon receptor engagement, JAK–STAT signaling is activated, promoting transcription of interferon-stimulated genes that shape epithelial barrier immunity and antiviral programs at mucosal surfaces. IL-28R expression and signaling intensity can influence inflammatory tone, susceptibility to viral infection, and the balance of innate and adaptive immune responses. Dysregulated IFNLR1 activity has been linked to variation in antiviral immunity and inflammatory phenotypes, making it a relevant target for mechanistic studies in infection and immunopathology models.
IL-28R Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IFNLR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IFNLR1. 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 IFNLR1 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 IFNLR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.