Lamin B receptor Double Nickase Plasmid (m): sc-430209-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Lamin B receptor 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
- Lamin B receptor Double Nickase Plasmid (m) and Lamin B receptor Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lbr. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Lamin B receptor Double Nickase Plasmid (m) | sc-430209-NIC | 20 µg | $410.00 | |||
Lamin B receptor Double Nickase Plasmid (m2) | sc-430209-NIC-2 | 20 µg | $410.00 |
Mouse Lbr encodes lamin B receptor, an integral protein of the inner nuclear membrane that binds B-type lamins and chromatin-associated factors to support nuclear envelope architecture and higher-order genome organization. Lamin B receptor contributes to heterochromatin tethering at the nuclear periphery, coupling nuclear lamina dynamics to DNA replication timing, transcriptional regulation, and mitotic reassembly of the nuclear envelope. Through these roles, Lbr is closely linked to pathways governing nuclear shape, chromatin compartmentalization, and lineage-specific gene expression programs. Perturbation of lamin–chromatin interactions is broadly relevant to studies of nuclear envelopathies and developmental phenotypes associated with altered nuclear morphology and genome regulation.
Lamin B receptor Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lbr locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lbr. 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 Lbr 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 Lbr-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.