ACSL6 Double Nickase Plasmid (h): sc-407772-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACSL6 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
- ACSL6 Double Nickase Plasmid (h) and ACSL6 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACSL6. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSL6 Double Nickase Plasmid (h) | sc-407772-NIC | 20 µg | $410.00 | |||
ACSL6 Double Nickase Plasmid (h2) | sc-407772-NIC-2 | 20 µg | $410.00 |
ACSL6 (acyl-CoA synthetase long-chain family member 6) catalyzes ATP-dependent activation of long-chain fatty acids to their acyl-CoA derivatives, a committed step that channels lipids into β-oxidation, phospholipid remodeling, and neutral lipid synthesis. By shaping the cellular acyl-CoA pool, ACSL6 influences membrane composition, energy metabolism, and lipid signaling pathways that intersect with mitochondrial function and oxidative stress responses. Expression is enriched in neural and hematopoietic contexts, supporting studies of tissue-specific lipid utilization and membrane dynamics. Dysregulated fatty acid activation and acyl-CoA flux are implicated in metabolic and neurobiological disease mechanisms, making ACSL6 a relevant target for investigating lipid-driven phenotypes in human cells.
ACSL6 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACSL6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACSL6. 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 ACSL6 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 ACSL6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.