LDLR Double Nickase Plasmid (m): sc-421408-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LDLR 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
- LDLR Double Nickase Plasmid (m) and LDLR Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ldlr. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LDLR Antibody (C7): sc-18823
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LDLR Double Nickase Plasmid (m) | sc-421408-NIC | 20 µg | $410.00 |
Mouse Ldlr encodes the low-density lipoprotein receptor (LDLR), a cell-surface endocytic receptor that clears circulating LDL particles through clathrin-mediated internalization in hepatocytes and other tissues. LDLR governs cholesterol uptake and contributes to lipid homeostasis by regulating intracellular sterol availability that feeds back on SREBP-controlled transcriptional programs and broader lipoprotein metabolism pathways. Disruption or reduced activity of LDLR is classically linked to dyslipidemia phenotypes and atherosclerosis-relevant biology, making Ldlr a central node for studying cholesterol trafficking and systemic lipid regulation in vivo and in cultured cells. Experimental perturbation of Ldlr is commonly used to interrogate LDL particle uptake kinetics, receptor recycling, and downstream sterol-responsive gene networks.
LDLR Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ldlr locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ldlr. 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 Ldlr 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 Ldlr-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.