BAF53B Double Nickase Plasmid (h): sc-409940-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BAF53B 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
- BAF53B Double Nickase Plasmid (h) and BAF53B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ACTL6B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BAF53B Double Nickase Plasmid (h) | sc-409940-NIC | 20 µg | $410.00 | |||
BAF53B Double Nickase Plasmid (h2) | sc-409940-NIC-2 | 20 µg | $410.00 |
Human ACTL6B encodes BAF53B, an actin-related subunit of neuron-enriched SWI/SNF (BAF) ATP-dependent chromatin remodeling complexes that regulate nucleosome positioning and transcriptional programs during neurodevelopment. BAF53B contributes to activity-dependent gene expression, neuronal differentiation, and synaptic plasticity by coordinating chromatin accessibility with transcription factor occupancy. Through its role in BAF complex assembly and targeting, ACTL6B links epigenetic regulation to pathways controlling neuronal maturation and circuit formation. Dysregulation of BAF complex components and neuronal chromatin remodeling is implicated in neurodevelopmental and neuropsychiatric disease mechanisms, making ACTL6B a useful locus for interrogating gene–chromatin relationships in brain-relevant models.
BAF53B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ACTL6B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ACTL6B. 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 ACTL6B 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 ACTL6B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.