IRF-2BP2 Double Nickase Plasmid (h): sc-406153-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IRF-2BP2 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
- IRF-2BP2 Double Nickase Plasmid (h) and IRF-2BP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IRF2BP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IRF-2BP2 Double Nickase Plasmid (h) | sc-406153-NIC | 20 µg | $410.00 | |||
IRF-2BP2 Double Nickase Plasmid (h2) | sc-406153-NIC-2 | 20 µg | $410.00 |
IRF2BP2 encodes IRF-2BP2, a transcriptional coregulator that associates with interferon regulatory factors and other DNA-binding proteins to tune context-dependent gene expression programs. Through modulation of interferon-responsive transcription and broader inflammatory signaling networks, IRF-2BP2 contributes to immune homeostasis, stress responses, and lineage-specific differentiation. Altered IRF2BP2 activity has been implicated in dysregulated cytokine signaling and transcriptional control relevant to inflammatory and cardiovascular phenotypes, as well as oncogenic transcriptional reprogramming reported in selected tumor contexts. These properties make IRF-2BP2 a useful node for dissecting innate immune regulation, transcription factor complexes, and stimulus-dependent gene regulatory circuitry in human cells.
IRF-2BP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IRF2BP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IRF2BP2. 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 IRF2BP2 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 IRF2BP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.