IL-11Rα Double Nickase Plasmid (h): sc-402503-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-11Rα 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
- IL-11Rα Double Nickase Plasmid (h) and IL-11Rα Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IL11RA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IL-11Rα Antibody (4D12): sc-130920
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-11Rα Double Nickase Plasmid (h) | sc-402503-NIC | 20 µg | $410.00 | |||
IL-11Rα Double Nickase Plasmid (h2) | sc-402503-NIC-2 | 20 µg | $410.00 |
IL11RA encodes the human interleukin-11 receptor alpha (IL-11Rα), a ligand-binding component that pairs with the GP130 co-receptor to initiate IL-11–dependent signaling. Upon cytokine engagement, this receptor complex activates JAK/STAT3 as well as MAPK/ERK and PI3K-associated pathways that regulate cell survival, differentiation, and tissue remodeling programs. IL-11Rα is studied in stromal and epithelial communication and in contexts where aberrant cytokine signaling contributes to inflammatory and fibrotic phenotypes. Dysregulated IL11RA pathway activity has also been linked to altered bone and craniofacial development, supporting its relevance in developmental biology and disease-modeling research.
IL-11Rα Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IL11RA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IL11RA. 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 IL11RA 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 IL11RA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.