BRCA1 Double Nickase Plasmid (m): sc-419362-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BRCA1 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
- BRCA1 Double Nickase Plasmid (m) and BRCA1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Brca1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BRCA1 Antibody (287.17): sc-135732
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BRCA1 Double Nickase Plasmid (m) | sc-419362-NIC | 20 µg | $410.00 | |||
BRCA1 Double Nickase Plasmid (m2) | sc-419362-NIC-2 | 20 µg | $410.00 |
Mouse Brca1 encodes BRCA1, a multifunctional tumor suppressor that coordinates high-fidelity DNA double-strand break repair through homologous recombination and promotes replication fork protection. BRCA1 operates in genome surveillance networks including ATM/ATR signaling and checkpoint control, and forms functional complexes with partners such as BARD1, PALB2, and BRCA2 to regulate end resection and RAD51 loading. Beyond DNA repair, BRCA1 influences chromatin remodeling and transcriptional responses to genotoxic stress, shaping cell-cycle progression and maintenance of genomic stability. Disruption of Brca1 is tightly linked to elevated DNA damage, chromosomal instability, and phenotypes relevant to cancer predisposition biology in mammalian systems.
BRCA1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Brca1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Brca1. 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 Brca1 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 Brca1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.