BRD9 Double Nickase Plasmid (h): sc-404933-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BRD9 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
- BRD9 Double Nickase Plasmid (h) and BRD9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BRD9. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BRD9 Double Nickase Plasmid (h) | sc-404933-NIC | 20 µg | $410.00 |
BRD9 encodes a bromodomain-containing chromatin reader that recognizes acetylated lysines on histones and contributes to transcriptional regulation by modulating chromatin accessibility. BRD9 is a defining component of non-canonical BAF (ncBAF) chromatin remodeling complexes, influencing enhancer activity, lineage-specific gene expression programs, and cell-cycle-associated transcription. Through these epigenetic functions, BRD9 participates in pathways governing proliferation, differentiation, and stress responses that are frequently perturbed in human disease. Dysregulated BRD9-dependent chromatin regulation has been investigated in cancer and other disorders with altered transcriptional control and chromatin remodeling.
BRD9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BRD9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BRD9. 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 BRD9 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 BRD9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.