BRCA2 Double Nickase Plasmid (m): sc-419363-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BRCA2 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
- BRCA2 Double Nickase Plasmid (m) and BRCA2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Brca2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BRCA2 Double Nickase Plasmid (m) | sc-419363-NIC | 20 µg | $410.00 | |||
BRCA2 Double Nickase Plasmid (m2) | sc-419363-NIC-2 | 20 µg | $410.00 |
Mouse Brca2 encodes BRCA2, a central mediator of homologous recombination that promotes RAD51 filament assembly and governs high-fidelity repair of DNA double-strand breaks. BRCA2 coordinates replication fork protection and recovery, helping to prevent replication stress–induced genome instability during S phase. Through its roles in DNA damage response signaling and chromatin-associated repair processes, BRCA2 supports proper chromosome segregation and suppresses accumulation of deleterious rearrangements. Disruption of BRCA2 function is widely used to model defective homology-directed repair, altered sensitivity to DNA damaging agents, and mutational processes linked to cancer predisposition biology.
BRCA2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Brca2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Brca2. 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 Brca2 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 Brca2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.