SEMA4A CRISPR/Cas9 KO Plasmid (m): sc-422880
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA4A 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 SEMA4A 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 | |
SEMA4A CRISPR/Cas9 KO Plasmid (m) | sc-422880 | 20 µg | $397.00 |
Overview
Sema4a encodes semaphorin-4A (SEMA4A), a membrane-associated guidance cue that also functions as an immunoregulatory ligand influencing cell–cell communication. In mice, SEMA4A contributes to axon guidance and synapse organization while modulating T cell activation, differentiation, and antigen-presenting cell interactions through semaphorin signaling networks and receptor-mediated pathways. These processes intersect with cytoskeletal remodeling, cell migration, and inflammatory signaling programs that shape tissue homeostasis. Dysregulated Sema4a activity has been associated with immune-driven pathology and neuroinflammatory mechanisms, supporting its study in models of autoimmunity, neurobiology, and barrier tissue inflammation.
SEMA4A CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sema4a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sema4a 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 Sema4a 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 SEMA4A protein expression.
This CRISPR knockout system enables efficient generation of Sema4a-deficient cell models for investigation of SEMA4A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sema4a exon(s) critical for SEMA4A 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 Sema4a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SEMA4A CRISPR/Cas9 KO Plasmid (m) and SEMA4A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sema4a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SEMA4A HDR Plasmid (m) and SEMA4A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sema4a homology arms to support homology-directed repair at defined Sema4a 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.