ACSL1 Double Nickase Plasmid (m): sc-420278-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACSL1 Double Nickase Plasmid (m) 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
- ACSL1 Double Nickase Plasmid (m) and ACSL1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Acsl1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSL1 Double Nickase Plasmid (m) | sc-420278-NIC | 20 µg | $410.00 |
Mouse Acsl1 encodes acyl-CoA synthetase long-chain family member 1 (ACSL1), an enzyme that converts long-chain free fatty acids into their corresponding acyl-CoA thioesters, a gating step that commits lipids to downstream metabolism. ACSL1 supports mitochondrial β-oxidation, lipid storage and remodeling, and broader energy homeostasis by controlling acyl-CoA availability for pathways including triglyceride synthesis, phospholipid turnover, and fatty acid catabolism. In metabolically active tissues and immune cell contexts, ACSL1 activity influences lipid-driven signaling and inflammatory programs, linking Acsl1 regulation to metabolic stress responses. Altered ACSL1 expression or activity is associated with dysregulated lipid metabolism phenotypes relevant to insulin resistance, steatosis, and cardiometabolic disease models in mice.
ACSL1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Acsl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Acsl1. 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 Acsl1 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 Acsl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.