IKKβ Double Nickase Plasmid (m): sc-421074-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IKKβ 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
- IKKβ Double Nickase Plasmid (m) and IKKβ Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ikbkb. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IKKβ Double Nickase Plasmid (m) | sc-421074-NIC | 20 µg | $410.00 | |||
IKKβ Double Nickase Plasmid (m2) | sc-421074-NIC-2 | 20 µg | $410.00 |
Ikbkb encodes the catalytic subunit IKKβ (IKKβ), a core component of the IKK complex that phosphorylates IκB proteins to promote their ubiquitination and degradation, enabling NF-κB nuclear translocation and transcriptional responses. Through canonical NF-κB signaling, IKKβ integrates inputs from cytokine receptors such as TNFR and IL-1R, pattern-recognition receptors, and cellular stress pathways to regulate inflammation, innate immunity, and survival programs. Dysregulated IKKβ activity is widely used as a molecular entry point for studying chronic inflammatory signaling, immune cell activation states, and stress-adaptive transcriptional networks in mouse models. Ikbkb perturbation is also relevant to mechanistic research on oncogenic inflammation, metabolic dysfunction, and neuroinflammatory processes where NF-κB pathway tone shapes cellular phenotypes.
IKKβ Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ikbkb locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ikbkb. 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 Ikbkb 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 Ikbkb-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.