LGR5 Double Nickase Plasmid (m): sc-420320-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LGR5 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
- LGR5 Double Nickase Plasmid (m) and LGR5 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lgr5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LGR5 Double Nickase Plasmid (m) | sc-420320-NIC | 20 µg | $410.00 | |||
LGR5 Double Nickase Plasmid (m2) | sc-420320-NIC-2 | 20 µg | $410.00 |
Lgr5 encodes leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5), a key marker of adult stem cell populations and a potentiator of WNT/β-catenin signaling through binding R-spondin ligands. In mouse tissues, LGR5-positive cells contribute to epithelial homeostasis and regeneration by influencing self-renewal, lineage commitment, and proliferative programs. LGR5 activity interfaces with pathways governing stemness and differentiation, including WNT-driven transcriptional networks and tissue-specific niche signals. Dysregulated Lgr5 expression or signaling is frequently examined in models of aberrant crypt/villus dynamics, tumor initiation biology, and organoid growth behavior without implying clinical outcomes.
LGR5 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lgr5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lgr5. 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 Lgr5 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 Lgr5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.