CYP11A1 Double Nickase Plasmid (h): sc-401269-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CYP11A1 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
- CYP11A1 Double Nickase Plasmid (h) and CYP11A1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CYP11A1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYP11A1 Double Nickase Plasmid (h) | sc-401269-NIC | 20 µg | $410.00 | |||
CYP11A1 Double Nickase Plasmid (h2) | sc-401269-NIC-2 | 20 µg | $410.00 |
CYP11A1 encodes the mitochondrial cytochrome P450 side-chain cleavage enzyme (P450scc), which catalyzes conversion of cholesterol to pregnenolone, the first and rate-limiting step of steroid hormone biosynthesis. This reaction initiates the production of glucocorticoids, mineralocorticoids, and sex steroids and integrates with mitochondrial cholesterol transport and redox partner pathways involving ferredoxin and ferredoxin reductase. CYP11A1 activity is central to steroidogenic programs in adrenal cortex and gonadal tissues, linking to endocrine homeostasis and cellular differentiation states. Altered CYP11A1 expression or function is associated with congenital steroid biosynthesis disorders, adrenal insufficiency phenotypes, and dysregulated steroidogenic signaling studied in reproductive and adrenal disease models.
CYP11A1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CYP11A1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CYP11A1. 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 CYP11A1 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 CYP11A1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.