BRD7 Double Nickase Plasmid (h): sc-416299-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BRD7 Double Nickase Plasmid (h) 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
- BRD7 Double Nickase Plasmid (h) and BRD7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BRD7. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BRD7 Antibody (B-8): sc-376180
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BRD7 Double Nickase Plasmid (h) | sc-416299-NIC | 20 µg | $410.00 | |||
BRD7 Double Nickase Plasmid (h2) | sc-416299-NIC-2 | 20 µg | $410.00 |
BRD7 encodes a bromodomain-containing chromatin reader that binds acetylated histones and contributes to transcriptional control through nucleosome remodeling. It functions in the PBAF/SWI/SNF chromatin remodeling context and has been linked to regulation of cell-cycle progression, DNA damage responses, and stress-associated transcriptional programs. BRD7 also modulates signaling networks including p53- and PI3K/AKT-associated pathways, influencing proliferative and metabolic gene expression. Dysregulated BRD7 expression or altered chromatin occupancy has been reported in multiple tumor types, making it relevant for studies of epigenetic control, genome stability, and oncogenic transcriptional dependencies.
BRD7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BRD7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BRD7. 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 BRD7 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 BRD7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.