CPOX Double Nickase Plasmid (h): sc-405130-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CPOX 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
- CPOX Double Nickase Plasmid (h) and CPOX Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CPOX. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CPOX Antibody (B-9): sc-393388
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CPOX Double Nickase Plasmid (h) | sc-405130-NIC | 20 µg | $410.00 | |||
CPOX Double Nickase Plasmid (h2) | sc-405130-NIC-2 | 20 µg | $410.00 |
Human CPOX encodes coproporphyrinogen oxidase, a mitochondrial enzyme that catalyzes the oxidative decarboxylation of coproporphyrinogen III to protoporphyrinogen IX in the heme biosynthesis pathway. This step links cellular iron utilization, mitochondrial redox metabolism, and synthesis of heme required for hemoproteins involved in oxidative phosphorylation and detoxification reactions. Altered CPOX activity perturbs porphyrin homeostasis and can drive accumulation of porphyrin intermediates associated with photosensitivity and neurovisceral features in porphyria-related phenotypes. CPOX is therefore widely studied in mitochondrial biology, erythroid differentiation, and metabolic stress responses that influence heme-dependent signaling.
CPOX Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CPOX locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CPOX. 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 CPOX 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 CPOX-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.