BAF53B CRISPR/Cas9 KO Plasmid (h): sc-409940
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BAF53B CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the BAF53B genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BAF53B CRISPR/Cas9 KO Plasmid (h) | sc-409940 | 20 µg | $397.00 |
Overview
ACTL6B encodes BAF53B, an actin-related protein subunit of neuron-enriched SWI/SNF (BAF) ATP-dependent chromatin remodeling complexes that regulate nucleosome positioning and chromatin accessibility. BAF53B supports transcriptional programs required for neuronal differentiation, dendritic and synaptic maturation, and activity-dependent gene regulation by coordinating with other BAF components to modulate enhancer and promoter usage. Through these epigenetic functions, ACTL6B is linked to pathways controlling neurodevelopmental timing, neuronal connectivity, and plasticity. Genetic and functional perturbations of ACTL6B/BAF53B have been associated with neurodevelopmental disorders and altered neuronal gene expression states relevant to models of cognitive and behavioral phenotypes.
BAF53B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ACTL6B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ACTL6B together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the ACTL6B open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish BAF53B protein expression.
This CRISPR knockout system enables efficient generation of ACTL6B-deficient cell models for investigation of BAF53B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ACTL6B exon(s) critical for BAF53B function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple ACTL6B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BAF53B CRISPR/Cas9 KO Plasmid (h) and BAF53B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ACTL6B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BAF53B HDR Plasmid (h) and BAF53B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ACTL6B homology arms to support homology-directed repair at defined ACTL6B target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.