EphA7 CRISPR/Cas9 KO Plasmid (m): sc-420197
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- EphA7 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 EphA7 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: EphA7 Antibody (E-7): sc-393973
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EphA7 CRISPR/Cas9 KO Plasmid (m) | sc-420197 | 20 µg | $397.00 |
Overview
Epha7 encodes EphA7, a receptor tyrosine kinase in the Eph/ephrin family that mediates contact-dependent signaling to regulate cell positioning, adhesion, and repulsive guidance during development. EphA7 activation influences cytoskeletal remodeling and downstream pathways such as Rho-family GTPase signaling, MAPK/ERK, and PI3K-dependent processes that shape migration, boundary formation, and axon targeting. In mouse tissues, EphA7 is implicated in neural patterning and circuit assembly, where altered Eph/ephrin signaling can perturb connectivity and tissue organization. Dysregulated EphA7-associated signaling has been studied in models of neurodevelopmental abnormalities and tumor biology through effects on proliferation, invasion, and microenvironmental interactions.
EphA7 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Epha7 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Epha7 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 Epha7 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 EphA7 protein expression.
This CRISPR knockout system enables efficient generation of Epha7-deficient cell models for investigation of EphA7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Epha7 exon(s) critical for EphA7 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 Epha7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by EphA7 CRISPR/Cas9 KO Plasmid (m) and EphA7 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Epha7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by EphA7 HDR Plasmid (m) and EphA7 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Epha7 homology arms to support homology-directed repair at defined Epha7 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.