COX11 Double Nickase Plasmid (h): sc-405874-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- COX11 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
- COX11 Double Nickase Plasmid (h) and COX11 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting COX11. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
COX11 Double Nickase Plasmid (h) | sc-405874-NIC | 20 µg | $410.00 | |||
COX11 Double Nickase Plasmid (h2) | sc-405874-NIC-2 | 20 µg | $410.00 |
Human COX11 encodes a conserved mitochondrial inner membrane copper chaperone required for cytochrome c oxidase (complex IV) biogenesis. COX11 participates in copper delivery to the CuB center of MT-CO1, supporting oxidative phosphorylation, electron transport, and efficient ATP production. Disruption of COX11 perturbs respiratory chain assembly and elevates mitochondrial stress responses that influence redox homeostasis and metabolic reprogramming. Altered complex IV maturation and mitochondrial dysfunction associated with COX11-linked pathways are relevant to studies of neurodegeneration, myopathies, and cancer cell bioenergetics.
COX11 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the COX11 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within COX11. 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 COX11 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 COX11-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.