β1-Adaptin CRISPR/Cas9 KO Plasmid (h): sc-402948
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β1-Adaptin 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 β1-Adaptin 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 | |
β1-Adaptin CRISPR/Cas9 KO Plasmid (h) | sc-402948 | 20 µg | $397.00 |
Overview
AP1B1 encodes β1-Adaptin, the β subunit of the adaptor protein complex 1 (AP-1) that couples cargo recognition to clathrin-mediated vesicle formation at the trans-Golgi network and endosomes. By binding sorting motifs on transmembrane proteins and coordinating with small GTPases and accessory factors, AP-1 regulates polarized trafficking, endosomal recycling, and lysosome-directed transport that support membrane composition and signaling homeostasis. Disruption of AP1B1-dependent sorting perturbs epithelial polarity and can alter receptor distribution, nutrient transporter localization, and proteostasis pathways linked to cellular stress responses. Genetic variation in AP1B1 has been associated with neurodevelopmental and trafficking-related phenotypes, making it relevant for mechanistic studies of vesicle transport dysfunction.
β1-Adaptin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the AP1B1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the AP1B1 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 AP1B1 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 β1-Adaptin protein expression.
This CRISPR knockout system enables efficient generation of AP1B1-deficient cell models for investigation of β1-Adaptin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting AP1B1 exon(s) critical for β1-Adaptin 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 AP1B1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by β1-Adaptin CRISPR/Cas9 KO Plasmid (h) and β1-Adaptin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the AP1B1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by β1-Adaptin HDR Plasmid (h) and β1-Adaptin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by AP1B1 homology arms to support homology-directed repair at defined AP1B1 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.