BRCA1 Double Nickase Plasmid (r): sc-437320-NIC
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BRCA1 Double Nickase Plasmid (r) 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 (r) and BRCA1 Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . 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 (r) | sc-437320-NIC | 20 µg | $410.00 | |||
BRCA1 Double Nickase Plasmid (r2) | sc-437320-NIC-2 | 20 µg | $410.00 |
BRCA1 encodes a multifunctional tumor suppressor that orchestrates genome maintenance by coordinating homologous recombination repair of DNA double-strand breaks, replication fork protection, and cell-cycle checkpoint control. In rat cells, BRCA1 functions within the BRCA1–PALB2–BRCA2 axis to promote RAD51 loading and participates in DNA damage signaling pathways governed by ATM/ATR kinases. Loss or impairment of BRCA1 disrupts chromatin-associated repair processes, elevates genomic instability, and sensitizes cells to replication stress. These mechanisms make BRCA1 a central node for studying DNA repair pathway choice, mitotic fidelity, and cancer-relevant genome integrity phenotypes in rodent models.
BRCA1 Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.