IL-3Rα Double Nickase Plasmid (h): sc-437304-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-3Rα 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-3Rα Double Nickase Plasmid (h) and IL-3Rα Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IL3RA. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-3Rα Double Nickase Plasmid (h) | sc-437304-NIC | 20 µg | $410.00 |
IL3RA encodes the interleukin-3 receptor alpha chain (IL-3Rα, CD123), the ligand-binding component of the IL-3 receptor complex that heterodimerizes with the common beta chain (CSF2RB) to initiate signaling. IL-3Rα engagement supports survival, proliferation, and differentiation programs in hematopoietic progenitors and myeloid lineage cells, with downstream activation of JAK/STAT, PI3K–AKT, and RAS–MAPK pathways. Altered IL3RA expression is used to study dysregulated cytokine signaling, lineage commitment, and immune cell homeostasis in hematologic disease contexts. As a cell-surface receptor with restricted expression patterns, IL-3Rα is frequently investigated as a marker and functional driver in models of aberrant myeloid biology and inflammatory signaling.
IL-3Rα Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IL3RA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IL3RA. 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 IL3RA 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 IL3RA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.