ACSL1 Double Nickase Plasmid (h): sc-402922-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACSL1 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
- ACSL1 Double Nickase Plasmid (h) and ACSL1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACSL1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ACSL1 Antibody (3G4): sc-293281
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSL1 Double Nickase Plasmid (h) | sc-402922-NIC | 20 µg | $410.00 | |||
ACSL1 Double Nickase Plasmid (h2) | sc-402922-NIC-2 | 20 µg | $410.00 |
ACSL1 (acyl‑CoA synthetase long‑chain family member 1) catalyzes the ATP‑dependent activation of long‑chain fatty acids to acyl‑CoA, a committed step that channels lipids toward mitochondrial β‑oxidation, triglyceride and phospholipid synthesis, and lipid‑derived signaling. By controlling acyl‑CoA pool composition, ACSL1 influences membrane remodeling, lipid droplet dynamics, and metabolic coupling between fatty acid uptake and downstream oxidation or storage pathways. Its activity is tightly linked to PPAR-regulated metabolic programs and broader networks governing insulin sensitivity, inflammation, and cellular energy homeostasis. Altered ACSL1 expression or regulation has been associated with metabolic dysregulation and lipid‑driven phenotypes relevant to obesity, type 2 diabetes, and cardiovascular biology, supporting mechanistic studies in disease-relevant cell models.
ACSL1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACSL1 locus in human 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.