LRP4 Double Nickase Plasmid (h): sc-401708-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRP4 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
- LRP4 Double Nickase Plasmid (h) and LRP4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LRP4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LRP4 Double Nickase Plasmid (h) | sc-401708-NIC | 20 µg | $410.00 | |||
LRP4 Double Nickase Plasmid (h2) | sc-401708-NIC-2 | 20 µg | $410.00 |
LRP4 (low-density lipoprotein receptor–related protein 4) is a single-pass transmembrane receptor of the LDL receptor family that functions as a key scaffold for extracellular ligand interactions and signal transduction at the cell surface. In the neuromuscular junction, LRP4 binds agrin and cooperates with MuSK to initiate receptor clustering and postsynaptic specialization, linking extracellular cues to cytoskeletal organization and synaptogenesis. In bone biology, LRP4 modulates Wnt/β-catenin signaling by interacting with secreted Wnt antagonists such as sclerostin and DKK1, influencing osteoblast activity and bone mass regulation. Genetic perturbations of LRP4 have been associated with congenital neuromuscular and skeletal phenotypes, making it a relevant target for studying synaptic development and bone remodeling mechanisms.
LRP4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LRP4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LRP4. 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 LRP4 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 LRP4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.