EphB2 CRISPR/Cas9 KO Plasmid (m): sc-420199
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EphB2 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 EphB2 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: EphB2 Antibody (2D12C6): sc-130068
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EphB2 CRISPR/Cas9 KO Plasmid (m) | sc-420199 | 20 µg | $397.00 |
Overview
Ephb2 encodes EphB2, a receptor tyrosine kinase in the ephrin–Eph signaling system that mediates contact-dependent communication between neighboring cells. Upon binding membrane-tethered ephrin-B ligands, EphB2 triggers bidirectional signaling that regulates cytoskeletal remodeling, cell adhesion, and directional migration, with prominent roles in axon guidance, synapse organization, and tissue boundary formation. In mouse models, EphB2-dependent signaling influences neuronal circuit assembly and vascular patterning and has been linked to phenotypes involving altered cell positioning and invasive behavior. Dysregulated EphB2 activity is frequently studied in the context of developmental defects and cancer-related pathways that control motility and compartmentalization.
EphB2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ephb2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ephb2 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 Ephb2 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 EphB2 protein expression.
This CRISPR knockout system enables efficient generation of Ephb2-deficient cell models for investigation of EphB2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ephb2 exon(s) critical for EphB2 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 Ephb2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by EphB2 CRISPR/Cas9 KO Plasmid (m) and EphB2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ephb2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by EphB2 HDR Plasmid (m) and EphB2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ephb2 homology arms to support homology-directed repair at defined Ephb2 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.