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-γRα Double Nickase Plasmid (h): sc-401191-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-γRα 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-γRα Double Nickase Plasmid (h) and IFN-γRα Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IFNGR1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IFN-γRα Antibody (GIR-94): sc-12755
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-γRα Double Nickase Plasmid (h) | sc-401191-NIC | 20 µg | $410.00 | |||
IFN-γRα Double Nickase Plasmid (h2) | sc-401191-NIC-2 | 20 µg | $410.00 |
IFNGR1 encodes interferon gamma receptor alpha (IFN-γRα), the ligand-binding chain of the IFN-γ receptor complex that initiates antimicrobial and immunomodulatory signaling in response to IFN-γ. Upon receptor engagement, associated JAK1/JAK2 kinases phosphorylate STAT1 to drive transcriptional programs controlling antigen presentation, macrophage activation, and regulation of Th1-type immune responses. This axis intersects with innate immune sensing and inflammatory networks, influencing expression of interferon-stimulated genes and feedback regulators such as SOCS proteins. Dysregulation or loss of IFNGR1 function is linked to impaired IFN-γ responsiveness and altered host defense phenotypes, making it a key target for studying immune signaling defects and inflammatory disease mechanisms in human cells.
IFN-γRα Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IFNGR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IFNGR1. 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 IFNGR1 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 IFNGR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.