CPTI Double Nickase Plasmid (h): sc-401811-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CPTI 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
- CPTI Double Nickase Plasmid (h) and CPTI Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CPT1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CPTI Double Nickase Plasmid (h) | sc-401811-NIC | 20 µg | $410.00 | |||
CPTI Double Nickase Plasmid (h2) | sc-401811-NIC-2 | 20 µg | $410.00 |
CPT1A encodes carnitine palmitoyltransferase 1A (CPTI), the rate-limiting enzyme that transfers long-chain acyl groups to carnitine to enable mitochondrial import and β-oxidation. By controlling fatty acid flux into mitochondria, CPTI coordinates lipid catabolism with cellular energy balance and intersects with AMPK signaling, PPAR-regulated transcriptional programs, and ketogenesis during nutrient stress. Altered CPT1A activity has been linked to inborn errors of fatty acid oxidation and metabolic phenotypes involving hepatic lipid handling and glucose homeostasis. In cancer and immune cell biology, CPT1A-dependent fatty acid oxidation is frequently studied as a determinant of redox control, survival under metabolic stress, and lineage-specific bioenergetic states.
CPTI Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CPT1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CPT1A. 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 CPT1A 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 CPT1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.