LRP1B Double Nickase Plasmid (h): sc-404088-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRP1B 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
- LRP1B Double Nickase Plasmid (h) and LRP1B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LRP1B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LRP1B Antibody (1642CT736.5.59): sc-517340
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LRP1B Double Nickase Plasmid (h) | sc-404088-NIC | 20 µg | $410.00 | |||
LRP1B Double Nickase Plasmid (h2) | sc-404088-NIC-2 | 20 µg | $410.00 |
LRP1B encodes a large endocytic receptor of the LDL receptor family that participates in clathrin-mediated internalization and trafficking of extracellular ligands and receptor complexes. Through its roles in membrane turnover and receptor recycling, LRP1B can influence cell-surface protease activity, extracellular matrix interactions, and downstream signaling networks linked to cell adhesion and migration. Altered LRP1B function has been associated with disrupted cellular homeostasis and genome instability signatures observed across multiple tumor types. As a result, LRP1B is frequently studied in the context of epithelial biology, cancer genetics, and mechanisms governing receptor-mediated uptake and signaling modulation.
LRP1B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LRP1B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LRP1B. 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 LRP1B 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 LRP1B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.