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.
IL-4Rα Double Nickase Plasmid (m): sc-421111-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-4Rα 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-4Rα Double Nickase Plasmid (m) and IL-4Rα Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Il4ra. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IL-4Rα Antibody (H-4): sc-28361
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-4Rα Double Nickase Plasmid (m) | sc-421111-NIC | 20 µg | $410.00 | |||
IL-4Rα Double Nickase Plasmid (m2) | sc-421111-NIC-2 | 20 µg | $410.00 |
Il4ra encodes the mouse interleukin-4 receptor alpha chain (IL-4Rα), a shared receptor subunit for IL-4 and IL-13 that integrates signaling in type 2 immunity. Upon ligand binding and receptor complex formation, IL-4Rα activates JAK/STAT pathways, prominently STAT6, to regulate transcriptional programs controlling lymphocyte differentiation, macrophage polarization, epithelial responses, and immunoglobulin class switching. IL-4Rα-dependent signaling shapes allergic inflammation, airway hyperresponsiveness, and fibrotic remodeling, and it is also relevant to immune regulation in host defense and tumor-associated myeloid cell phenotypes. Dysregulated IL-4/IL-13–IL-4Rα activity has been implicated in experimental models of asthma, dermatitis, and other Th2-skewed inflammatory conditions.
IL-4Rα Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Il4ra locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Il4ra. 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 Il4ra 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 Il4ra-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.