Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CYP3A4 Double Nickase Plasmid (h): sc-416463-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CYP3A4 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
- CYP3A4 Double Nickase Plasmid (h) and CYP3A4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CYP3A4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CYP3A4 Antibody (HL3): sc-53850
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CYP3A4 Double Nickase Plasmid (h) | sc-416463-NIC | 20 µg | $410.00 | |||
CYP3A4 Double Nickase Plasmid (h2) | sc-416463-NIC-2 | 20 µg | $410.00 |
CYP3A4 encodes a heme-thiolate cytochrome P450 monooxygenase that catalyzes oxidative metabolism of a wide range of xenobiotics and endogenous substrates, including steroids, bile acids, and fatty acids. It functions primarily in the endoplasmic reticulum and integrates into hepatic and intestinal drug-metabolism networks, coordinating Phase I biotransformation with downstream detoxification and transport pathways. CYP3A4 activity is regulated by nuclear receptor signaling, including PXR and CAR, linking exposure-responsive transcriptional programs to metabolic capacity. Interindividual variation in CYP3A4 expression or function is a major determinant of drug–drug interactions and altered metabolic phenotypes studied in liver disease, inflammation, and cancer-associated metabolic reprogramming contexts.
CYP3A4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CYP3A4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CYP3A4. 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 CYP3A4 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 CYP3A4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.