bassoon CRISPR/Cas9 KO Plasmid (h): sc-406918
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- bassoon 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 bassoon 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: bassoon Antibody (SAP7F407): sc-58509
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
bassoon CRISPR/Cas9 KO Plasmid (h) | sc-406918 | 20 µg | $397.00 |
Overview
BSN encodes bassoon, a large presynaptic cytomatrix scaffold protein that organizes the active zone and supports efficient neurotransmitter release. Bassoon contributes to synaptic vesicle docking and priming, coupling synaptic vesicle pools to voltage-gated Ca²⁺ influx and coordinating interactions with other active zone components during synaptogenesis and synaptic maintenance. Through its role in presynaptic assembly and vesicle cycle dynamics, BSN is studied in pathways governing neuronal connectivity, synaptic plasticity, and activity-dependent neurotransmission. Altered bassoon-associated synaptic organization has been investigated in the context of neurodevelopmental and neuropsychiatric disease mechanisms where presynaptic dysfunction is a common cellular phenotype.
bassoon CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the BSN gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the BSN 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 BSN 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 bassoon protein expression.
This CRISPR knockout system enables efficient generation of BSN-deficient cell models for investigation of bassoon signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting BSN exon(s) critical for bassoon 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 BSN genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by bassoon CRISPR/Cas9 KO Plasmid (h) and bassoon CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the BSN locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by bassoon HDR Plasmid (h) and bassoon HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by BSN homology arms to support homology-directed repair at defined BSN 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.