IL-12Rβ2 Double Nickase Plasmid (m): sc-421085-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-12Rβ2 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
- IL-12Rβ2 Double Nickase Plasmid (m) and IL-12Rβ2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Il12rb2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-12Rβ2 Double Nickase Plasmid (m) | sc-421085-NIC | 20 µg | $410.00 | |||
IL-12Rβ2 Double Nickase Plasmid (m2) | sc-421085-NIC-2 | 20 µg | $410.00 |
Mouse Il12rb2 encodes interleukin-12 receptor subunit beta 2 (IL-12Rβ2), a signaling component of the heterodimeric IL-12 receptor expressed primarily on activated T cells and NK cells. Upon IL-12 binding, IL-12Rβ2 couples to JAK2 and promotes STAT4 phosphorylation, driving Th1 polarization, IFN-γ production, and cytotoxic lymphocyte effector programs. This axis integrates with innate and adaptive immune circuits that regulate cell-mediated immunity, antigen-driven inflammation, and cytokine cross-talk. Altered IL-12Rβ2 signaling has been associated with dysregulated Th1 responses and immune-pathway perturbations relevant to infection models, inflammatory disease mechanisms, and tumor immunology research.
IL-12Rβ2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Il12rb2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Il12rb2. 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 Il12rb2 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 Il12rb2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.