IFN-γR2 Double Nickase Plasmid (m): sc-421052-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IFN-γR2 Double Nickase Plasmid (m) 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-γR2 Double Nickase Plasmid (m) and IFN-γR2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ifngr2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IFN-γR2 Double Nickase Plasmid (m) | sc-421052-NIC | 20 µg | $410.00 | |||
IFN-γR2 Double Nickase Plasmid (m2) | sc-421052-NIC-2 | 20 µg | $410.00 |
Ifngr2 encodes the mouse interferon-γ receptor 2 (IFN-γR2), an essential signaling subunit of the heterodimeric IFN-γ receptor complex that enables cellular responsiveness to IFN-γ. Upon ligand engagement with IFNGR1/IFNGR2, associated JAK kinases activate STAT1 to induce interferon-stimulated gene programs that shape antigen presentation, macrophage activation, and cell-intrinsic antimicrobial defenses. This pathway coordinates innate and adaptive immunity, influencing leukocyte differentiation and cytokine networks. Dysregulated IFN-γ–JAK/STAT signaling is linked to inflammatory and autoimmune phenotypes and can alter host–pathogen interactions, making Ifngr2 a key node for immunology and infection research.
IFN-γR2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ifngr2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ifngr2. 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 Ifngr2 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 Ifngr2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.