LAL Double Nickase Plasmid (m): sc-421438-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LAL 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
- LAL Double Nickase Plasmid (m) and LAL Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lipa. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LAL Antibody (9G7F12): sc-58374
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LAL Double Nickase Plasmid (m) | sc-421438-NIC | 20 µg | $410.00 | |||
LAL Double Nickase Plasmid (m2) | sc-421438-NIC-2 | 20 µg | $410.00 |
Mouse Lipa encodes lysosomal acid lipase (LAL), a hydrolase that cleaves cholesteryl esters and triglycerides within lysosomes to generate free cholesterol and fatty acids. This activity supports intracellular lipid turnover, cholesterol trafficking, and metabolic homeostasis, influencing lysosome function and lipid-responsive signaling programs. LAL-dependent lipid catabolism interfaces with pathways governing lipoprotein handling, autophagy-lysosome dynamics, and inflammatory responses to lipid accumulation. Disruption of Lipa/LAL function is commonly studied in the context of lysosomal lipid storage phenotypes and downstream metabolic stress mechanisms relevant to hepatic and immune cell biology.
LAL Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lipa locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lipa. 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 Lipa 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 Lipa-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.