ACSL5 Double Nickase Plasmid (h): sc-403876-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACSL5 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
- ACSL5 Double Nickase Plasmid (h) and ACSL5 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACSL5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACSL5 Antibody (A-2): sc-365478
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSL5 Double Nickase Plasmid (h) | sc-403876-NIC | 20 µg | $410.00 | |||
ACSL5 Double Nickase Plasmid (h2) | sc-403876-NIC-2 | 20 µg | $410.00 |
ACSL5 encodes a long-chain acyl-CoA synthetase that activates fatty acids by converting them to acyl-CoA thioesters, a key entry step for lipid utilization and remodeling. By channeling substrates into mitochondrial β-oxidation, triglyceride synthesis, and phospholipid remodeling, ACSL5 influences cellular energy balance and membrane composition. Its activity intersects with metabolic stress responses and lipid-driven signaling pathways that regulate proliferation, apoptosis, and inflammatory programs. Dysregulated ACSL5 expression or function has been associated with altered lipid homeostasis in metabolic disease contexts and has been explored in relation to tumor cell metabolism and mitochondrial-dependent cell fate decisions.
ACSL5 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACSL5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACSL5. 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 ACSL5 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 ACSL5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.