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.
ICSBP Double Nickase Plasmid (h): sc-400774-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ICSBP 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
- ICSBP Double Nickase Plasmid (h) and ICSBP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting IRF8. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ICSBP Antibody (E-9): sc-365042
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ICSBP Double Nickase Plasmid (h) | sc-400774-NIC | 20 µg | $410.00 | |||
ICSBP Double Nickase Plasmid (h2) | sc-400774-NIC-2 | 20 µg | $410.00 |
Interferon regulatory factor 8 (IRF8), also known as ICSBP, is a hematopoietic transcription factor that governs lineage commitment and maturation of myeloid and dendritic cell populations. It integrates interferon and Toll-like receptor signaling by partnering with ETS/IRF family factors to modulate ISRE/EICE-containing promoters, shaping cytokine programs, antigen presentation, and innate immune effector functions. IRF8-dependent transcriptional networks influence macrophage polarization, dendritic cell development, and inflammatory gene expression, linking it to pathways controlling antimicrobial responses and immune homeostasis. Dysregulated IRF8 activity has been associated with altered myelopoiesis and immune dysfunction, and it is frequently studied in the context of leukemogenesis, myelodysplastic syndromes, and inflammatory disorders.
ICSBP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the IRF8 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within IRF8. 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 IRF8 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 IRF8-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.