caspase-11 Double Nickase Plasmid (m): sc-419462-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- caspase-11 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
- caspase-11 Double Nickase Plasmid (m) and caspase-11 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Casp4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: caspase-11 p20 Antibody (A-2): sc-374615
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
caspase-11 Double Nickase Plasmid (m) | sc-419462-NIC | 20 µg | $410.00 | |||
caspase-11 Double Nickase Plasmid (m2) | sc-419462-NIC-2 | 20 µg | $410.00 |
Mouse Casp4 encodes caspase-11, an inflammatory cysteine protease that functions as a cytosolic sensor of lipopolysaccharide and a key initiator of the noncanonical inflammasome pathway. Upon activation, caspase-11 cleaves gasdermin D to drive pyroptotic cell death and promotes maturation of inflammatory cytokine signaling through crosstalk with canonical inflammasome components. This axis integrates innate immune detection with membrane permeabilization, alarmin release, and downstream NF-κB–linked transcriptional programs. Dysregulated caspase-11 activity is widely used to model mechanisms of endotoxemia, inflammatory tissue injury, and host–pathogen interactions in macrophages and other myeloid lineages.
caspase-11 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Casp4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Casp4. 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 Casp4 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 Casp4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.