BCDO2 Double Nickase Plasmid (h): sc-413515-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BCDO2 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
- BCDO2 Double Nickase Plasmid (h) and BCDO2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BCO2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BCDO2 Double Nickase Plasmid (h) | sc-413515-NIC | 20 µg | $410.00 | |||
BCDO2 Double Nickase Plasmid (h2) | sc-413515-NIC-2 | 20 µg | $410.00 |
BCO2 encodes β-carotene 9′,10′-oxygenase 2 (BCDO2), a mitochondrial carotenoid-cleaving enzyme that catalyzes oxidative cleavage of carotenoids to apocarotenoids, thereby regulating intracellular carotenoid levels and downstream retinoid-related signaling. By controlling carotenoid turnover, BCDO2 influences mitochondrial redox balance and can modulate oxidative stress responses linked to lipid metabolism and cellular homeostasis. Altered BCO2 activity has been associated with interindividual variation in carotenoid metabolism and has been investigated in the context of metabolic traits and oxidative stress–related cellular phenotypes. These properties make BCO2 a useful target for studying mitochondrial metabolism, reactive oxygen species handling, and apocarotenoid-dependent transcriptional programs in human cells.
BCDO2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BCO2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BCO2. 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 BCO2 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 BCO2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.