megalin/LRP2 Double Nickase Plasmid (m): sc-420631-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- megalin/LRP2 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
- megalin/LRP2 Double Nickase Plasmid (m) and megalin/LRP2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lrp2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: megalin/LRP2 Antibody (G-9): sc-515750
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
megalin/LRP2 Double Nickase Plasmid (m) | sc-420631-NIC | 20 µg | $410.00 |
Mouse Lrp2 encodes megalin/LRP2, a multiligand endocytic receptor of the LDL receptor family expressed prominently in absorptive epithelia such as renal proximal tubule and neuroepithelium. It drives clathrin-mediated uptake and trafficking of vitamins, lipoproteins, hormone–carrier complexes, and morphogens, coupling endocytosis to endosomal sorting and lysosomal processing. Through interactions with adaptor proteins and co-receptors, megalin influences epithelial polarity, nutrient homeostasis, and signaling pathways including retinoid, Sonic hedgehog, and TGF-β/BMP-related processes. Disrupted Lrp2 function is used to model developmental anomalies and renal tubular dysfunction phenotypes, supporting studies of congenital malformation pathways and epithelial transport defects.
megalin/LRP2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lrp2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lrp2. 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 Lrp2 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 Lrp2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.