CYP1B1 Double Nickase Plasmid (m): sc-419899-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CYP1B1 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
- CYP1B1 Double Nickase Plasmid (m) and CYP1B1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cyp1b1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYP1B1 Double Nickase Plasmid (m) | sc-419899-NIC | 20 µg | $410.00 | |||
CYP1B1 Double Nickase Plasmid (m2) | sc-419899-NIC-2 | 20 µg | $410.00 |
Mouse Cyp1b1 encodes the cytochrome P450 enzyme CYP1B1, a heme-thiolate monooxygenase that catalyzes oxidative metabolism of endogenous substrates and xenobiotics, including hydroxylation reactions relevant to steroid and retinoid homeostasis. CYP1B1 activity is linked to AHR-driven transcriptional programs and phase I metabolic pathways that shape cellular responses to environmental ligands and oxidative stress. Through its impact on redox balance and bioactive metabolite production, Cyp1b1 has been studied in the context of vascular biology, ocular development, and tissue-specific susceptibility to toxicant-induced injury. In mouse models, altered Cyp1b1 function can influence signaling networks downstream of metabolic intermediates, supporting mechanistic research on metabolism–inflammation and development-associated phenotypes.
CYP1B1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cyp1b1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cyp1b1. 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 Cyp1b1 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 Cyp1b1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.