BPTF Double Nickase Plasmid (m): sc-431488-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BPTF 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
- BPTF Double Nickase Plasmid (m) and BPTF Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Bptf. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BPTF Double Nickase Plasmid (m) | sc-431488-NIC | 20 µg | $410.00 | |||
BPTF Double Nickase Plasmid (m2) | sc-431488-NIC-2 | 20 µg | $410.00 |
Bptf encodes bromodomain PHD finger transcription factor (BPTF), a core subunit of the NURF chromatin remodeling complex that reads histone marks and regulates nucleosome positioning to control gene expression. In mouse cells, BPTF contributes to transcriptional programs governing proliferation, lineage specification, and developmental patterning by coordinating chromatin accessibility at promoters and enhancers. Through its bromodomain and PHD finger, BPTF integrates epigenetic signals with transcription factor networks, impacting processes such as DNA-templated transcription and chromatin organization. Dysregulated BPTF activity is implicated in altered chromatin states and aberrant transcriptional outputs relevant to cancer biology and other diseases involving epigenetic misregulation.
BPTF Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Bptf locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Bptf. 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 Bptf 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 Bptf-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.