LYCAT Double Nickase Plasmid (h): sc-415182-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LYCAT 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
- LYCAT Double Nickase Plasmid (h) and LYCAT Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LCLAT1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LYCAT Double Nickase Plasmid (h) | sc-415182-NIC | 20 µg | $410.00 |
LCLAT1 encodes lysocardiolipin acyltransferase 1 (LYCAT), a membrane-associated acyltransferase that remodels lysocardiolipin and other lysophospholipids to maintain mitochondrial membrane composition and bioenergetic function. Through cardiolipin remodeling and phospholipid reacylation, LYCAT supports mitochondrial respiratory chain organization, membrane curvature, and lipid-dependent signaling. Perturbation of LCLAT1 activity can shift cardiolipin acyl-chain profiles, influencing oxidative phosphorylation efficiency and cellular stress responses. These processes are relevant to research on mitochondrial dysfunction, metabolic reprogramming, and inflammation-associated phenotypes observed across diverse disease models.
LYCAT Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LCLAT1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LCLAT1. 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 LCLAT1 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 LCLAT1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.