BCMO1 Double Nickase Plasmid (h): sc-405374-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BCMO1 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
- BCMO1 Double Nickase Plasmid (h) and BCMO1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BCO1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BCMO1 Double Nickase Plasmid (h) | sc-405374-NIC | 20 µg | $410.00 | |||
BCMO1 Double Nickase Plasmid (h2) | sc-405374-NIC-2 | 20 µg | $410.00 |
Human BCO1 encodes β-carotene 15,15′-monooxygenase 1 (BCMO1), a cytosolic enzyme that catalyzes the central cleavage of dietary β-carotene to generate retinal, a direct precursor of retinoic acid. Through control of retinoid availability, BCMO1 influences retinoic acid–dependent transcriptional programs governing epithelial differentiation, embryonic development, and immune and metabolic homeostasis. BCO1 activity intersects with carotenoid uptake and lipid-handling pathways, linking nutrient status to nuclear receptor signaling. Altered carotenoid and retinoid metabolism has been associated with variability in vitamin A status and with traits relevant to ocular and metabolic physiology, making BCO1 a useful target for mechanistic studies.
BCMO1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BCO1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BCO1. 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 BCO1 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 BCO1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.