CETP Double Nickase Plasmid (h): sc-405829-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CETP 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
- CETP Double Nickase Plasmid (h) and CETP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CETP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CETP Double Nickase Plasmid (h) | sc-405829-NIC | 20 µg | $410.00 | |||
CETP Double Nickase Plasmid (h2) | sc-405829-NIC-2 | 20 µg | $410.00 |
Cholesteryl ester transfer protein (CETP) is a secreted glycoprotein that mediates the exchange of cholesteryl esters and triglycerides between HDL and apoB-containing lipoproteins, shaping plasma lipoprotein composition and reverse cholesterol transport. By regulating HDL remodeling and lipid flux, CETP influences cholesterol homeostasis, hepatic uptake pathways, and downstream inflammatory responses linked to metabolic stress. Genetic variation or altered CETP expression has been associated with changes in HDL-C levels and lipoprotein particle distribution, connecting CETP biology to cardiometabolic phenotypes and atherosclerosis-related mechanisms. These features make CETP a useful target for dissecting lipid transport networks and lipoprotein-driven signaling in human cell and tissue models.
CETP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CETP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CETP. 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 CETP 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 CETP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.