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.
IFN-α/βRα Double Nickase Plasmid (h): sc-401662-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-α/βRα 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
- IFN-α/βRα Double Nickase Plasmid (h) and IFN-α/βRα Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IFNAR1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IFN-α/βRα Antibody (H-11): sc-7391
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-α/βRα Double Nickase Plasmid (h) | sc-401662-NIC | 20 µg | $410.00 | |||
IFN-α/βRα Double Nickase Plasmid (h2) | sc-401662-NIC-2 | 20 µg | $410.00 |
IFNAR1 encodes interferon alpha/beta receptor alpha (IFN-α/βRα), a cell-surface subunit of the type I interferon receptor that binds IFN-α and IFN-β to initiate innate immune signaling. Ligand engagement promotes activation of the JAK1/TYK2 kinases and downstream STAT1/STAT2–IRF9 (ISGF3) complexes, driving transcription of interferon-stimulated genes that regulate antiviral defense, antigen presentation, and immune-cell crosstalk. IFNAR1 activity is also shaped by receptor internalization and ubiquitin-mediated turnover, influencing signaling amplitude and duration. Dysregulated type I interferon pathways involving IFNAR1 are widely studied in inflammatory and autoimmune contexts as well as tumor–immune interactions and host–pathogen response phenotypes.
IFN-α/βRα Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IFNAR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IFNAR1. 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 IFNAR1 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 IFNAR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.