SEMA3F CRISPR/Cas9 KO Plasmid (m): sc-422879
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA3F 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 SEMA3F 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 | |
SEMA3F CRISPR/Cas9 KO Plasmid (m) | sc-422879 | 20 µg | $397.00 |
Overview
Sema3f encodes semaphorin-3F (SEMA3F), a secreted guidance cue that signals primarily through neuropilin and plexin receptor complexes to regulate cytoskeletal dynamics, adhesion, and directional migration. By modulating Rho family GTPase activity and downstream actin remodeling, SEMA3F influences axon pathfinding, vascular patterning, and epithelial tissue organization. In the immune and stromal microenvironment, SEMA3F-dependent repulsive signaling can shape cell positioning and motility, intersecting with integrin, MAPK, and PI3K pathway outputs. Dysregulated SEMA3F signaling has been associated with altered angiogenic and invasive phenotypes in disease-relevant models, supporting its use in mechanistic studies of development and tumor biology.
SEMA3F CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sema3f gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sema3f 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 Sema3f 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 SEMA3F protein expression.
This CRISPR knockout system enables efficient generation of Sema3f-deficient cell models for investigation of SEMA3F signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sema3f exon(s) critical for SEMA3F 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 Sema3f genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SEMA3F CRISPR/Cas9 KO Plasmid (m) and SEMA3F CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sema3f locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SEMA3F HDR Plasmid (m) and SEMA3F HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sema3f homology arms to support homology-directed repair at defined Sema3f 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.