LXR alpha/NR1H3 Double Nickase Plasmid (m): sc-423616-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LXR alpha/NR1H3 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
- LXR alpha/NR1H3 Double Nickase Plasmid (m) and LXR alpha/NR1H3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Nr1h3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LXR alpha/NR1H3 Double Nickase Plasmid (m) | sc-423616-NIC | 20 µg | $410.00 | |||
LXR alpha/NR1H3 Double Nickase Plasmid (m2) | sc-423616-NIC-2 | 20 µg | $410.00 |
Nr1h3 encodes liver X receptor alpha (LXRα/NR1H3), a ligand-activated nuclear receptor that heterodimerizes with RXR to regulate transcriptional programs controlling cholesterol efflux, bile acid metabolism, and fatty acid synthesis. LXRα integrates oxysterol sensing with lipoprotein handling by modulating targets involved in reverse cholesterol transport and sterol homeostasis, and it intersects with inflammatory signaling in macrophages through transrepression mechanisms. In mouse models, altered Nr1h3 activity has been used to study dyslipidemia, atherosclerosis-relevant foam cell biology, hepatic steatosis, and metabolic inflammation. These functions make NR1H3 a key node for investigating immunometabolic crosstalk across liver, adipose tissue, and innate immune compartments.
LXR alpha/NR1H3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Nr1h3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Nr1h3. 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 Nr1h3 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 Nr1h3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.