SEMA4C CRISPR/Cas9 KO Plasmid (m): sc-422882
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA4C 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 SEMA4C 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: SEMA4C Antibody (37): sc-136445
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SEMA4C CRISPR/Cas9 KO Plasmid (m) | sc-422882 | 20 µg | $397.00 |
Overview
Sema4c encodes semaphorin-4C (SEMA4C), a transmembrane guidance molecule that signals through plexin receptors to regulate cell–cell communication, directional migration, and cytoskeletal remodeling. In mouse tissues, SEMA4C contributes to contact-dependent signaling events that shape neural patterning and influence immune cell interactions, linking semaphorin pathways to developmental and inflammatory processes. Downstream effects frequently converge on Rho family GTPase regulation and MAPK-associated programs that coordinate adhesion dynamics and motility. Altered semaphorin–plexin signaling has been associated with dysregulated tissue remodeling and immune microenvironment changes, supporting its study in disease-relevant models without implying therapeutic outcomes.
SEMA4C CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sema4c gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sema4c 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 Sema4c 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 SEMA4C protein expression.
This CRISPR knockout system enables efficient generation of Sema4c-deficient cell models for investigation of SEMA4C signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sema4c exon(s) critical for SEMA4C 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 Sema4c genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SEMA4C CRISPR/Cas9 KO Plasmid (m) and SEMA4C CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sema4c locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SEMA4C HDR Plasmid (m) and SEMA4C HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sema4c homology arms to support homology-directed repair at defined Sema4c 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.