ACADL Double Nickase Plasmid (h): sc-404535-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACADL 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
- ACADL Double Nickase Plasmid (h) and ACADL Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACADL. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACADL Double Nickase Plasmid (h) | sc-404535-NIC | 20 µg | $410.00 | |||
ACADL Double Nickase Plasmid (h2) | sc-404535-NIC-2 | 20 µg | $410.00 |
ACADL encodes long-chain acyl-CoA dehydrogenase, a mitochondrial flavoprotein that catalyzes the first dehydrogenation step in β-oxidation of long-chain fatty acids, linking lipid catabolism to oxidative phosphorylation and cellular energy balance. Its activity is integrated with mitochondrial fatty acid import and electron transfer via ETF/ETFDH, and contributes to metabolic flexibility in tissues with high oxidative demand. Dysregulated ACADL function is associated with impaired fatty acid oxidation, mitochondrial stress, and altered lipid signaling that can influence cardiometabolic and neuromuscular phenotypes. In cancer and metabolic research, ACADL is frequently examined for its role in rewiring fatty acid utilization and redox homeostasis.
ACADL Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACADL locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACADL. 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 ACADL 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 ACADL-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.