β2-Adaptin CRISPR/Cas9 KO Plasmid (m): sc-428053
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β2-Adaptin 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 β2-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 | |
β2-Adaptin CRISPR/Cas9 KO Plasmid (m) | sc-428053 | 20 µg | $397.00 |
Overview
Ap2b1 encodes the β2-adaptin subunit of the AP-2 adaptor complex, a core component of clathrin-mediated endocytosis in mouse cells. β2-Adaptin helps couple cargo selection at the plasma membrane to clathrin coat assembly, coordinating internalization and recycling of receptors, transporters, and signaling complexes. Through these functions, AP-2 influences membrane trafficking–dependent pathways such as receptor tyrosine kinase signaling, synaptic vesicle cycling, and cytoskeletal dynamics. Disruption of AP-2–mediated trafficking is broadly relevant to studies of neurobiology, metabolism, and oncogenic signaling networks where altered receptor turnover and endosomal sorting can reshape cell-state responses.
β2-Adaptin CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ap2b1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ap2b1 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 Ap2b1 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 β2-Adaptin protein expression.
This CRISPR knockout system enables efficient generation of Ap2b1-deficient cell models for investigation of β2-Adaptin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ap2b1 exon(s) critical for β2-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 Ap2b1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by β2-Adaptin CRISPR/Cas9 KO Plasmid (m) and β2-Adaptin CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ap2b1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by β2-Adaptin HDR Plasmid (m) and β2-Adaptin HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ap2b1 homology arms to support homology-directed repair at defined Ap2b1 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.