AP-3β CRISPR/Cas9 KO Plasmid (m): sc-419135
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AP-3β CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 AP-3β 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: AP-3β Antibody (3B4): sc-517083
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AP-3β CRISPR/Cas9 KO Plasmid (m) | sc-419135 | 20 µg | $397.00 |
Overview
Ap3b1 encodes the mouse AP-3 β subunit, a core component of the adaptor protein-3 complex that recognizes cargo sorting motifs and directs vesicle trafficking from endosomes and the trans-Golgi network to lysosomes and lysosome-related organelles. AP-3–dependent trafficking supports membrane protein delivery, organelle biogenesis, and regulated secretion pathways that are critical for neuronal and immune cell physiology. Disruption of AP-3 complex function has been linked to defects in synaptic vesicle protein sorting and altered endolysosomal homeostasis, providing a mechanistic connection to neurodevelopmental and immunological phenotypes observed in AP-3 pathway perturbation.
AP-3β CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ap3b1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ap3b1 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 Ap3b1 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 AP-3β protein expression.
This CRISPR knockout system enables efficient generation of Ap3b1-deficient cell models for investigation of AP-3β signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ap3b1 exon(s) critical for AP-3β 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 Ap3b1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by AP-3β CRISPR/Cas9 KO Plasmid (m) and AP-3β CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ap3b1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by AP-3β HDR Plasmid (m) and AP-3β HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ap3b1 homology arms to support homology-directed repair at defined Ap3b1 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.