Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
BBS4 CRISPR/Cas9 KO Plasmid (h): sc-403421
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BBS4 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 BBS4 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: BBS4 Antibody (1292CT845.130.218): sc-517315
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BBS4 CRISPR/Cas9 KO Plasmid (h) | sc-403421 | 20 µg | $397.00 |
Overview
BBS4 encodes a core component of the BBSome complex that cooperates with intraflagellar transport machinery to regulate primary cilium assembly and ciliary membrane protein trafficking. Through its role in ciliary signaling competence, BBS4 influences pathways such as Hedgehog and other receptor-mediated programs that depend on intact ciliogenesis and selective cargo delivery. Disruption of BBS4 perturbs centrosome/basal body function, compromises ciliary structure, and alters cellular responses to extracellular cues. Variants in BBS4 are associated with Bardet–Biedl syndrome and related ciliopathies, making it relevant for studying mechanisms linking ciliary dysfunction to developmental and metabolic phenotypes.
BBS4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the BBS4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the BBS4 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 BBS4 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 BBS4 protein expression.
This CRISPR knockout system enables efficient generation of BBS4-deficient cell models for investigation of BBS4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting BBS4 exon(s) critical for BBS4 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 BBS4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BBS4 CRISPR/Cas9 KO Plasmid (h) and BBS4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the BBS4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BBS4 HDR Plasmid (h) and BBS4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by BBS4 homology arms to support homology-directed repair at defined BBS4 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.