CYP11B2 Double Nickase Plasmid (h): sc-405281-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CYP11B2 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
- CYP11B2 Double Nickase Plasmid (h) and CYP11B2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CYP11B2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYP11B2 Double Nickase Plasmid (h) | sc-405281-NIC | 20 µg | $410.00 | |||
CYP11B2 Double Nickase Plasmid (h2) | sc-405281-NIC-2 | 20 µg | $410.00 |
CYP11B2 encodes aldosterone synthase, a mitochondrial cytochrome P450 enzyme that catalyzes the terminal oxidation steps converting 11-deoxycorticosterone to aldosterone in adrenal zona glomerulosa cells. Its activity links cholesterol-derived steroidogenesis to the renin–angiotensin–aldosterone system, integrating mitochondrial electron transfer, heme-dependent monooxygenation, and endocrine control of electrolyte and blood pressure homeostasis. Dysregulated CYP11B2 expression or activity is associated with aldosterone excess states, including primary aldosteronism and aldosterone-producing adrenal adenomas, and contributes to cardiovascular and renal pathophysiology. As a marker and driver of mineralocorticoid biosynthesis, CYP11B2 is widely studied in adrenal cell differentiation, angiotensin II signaling, and steroid metabolic flux.
CYP11B2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CYP11B2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CYP11B2. 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 CYP11B2 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 CYP11B2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.