SEMA4B CRISPR/Cas9 KO Plasmid (m): sc-422881
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA4B 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 SEMA4B 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 | |
SEMA4B CRISPR/Cas9 KO Plasmid (m) | sc-422881 | 20 µg | $397.00 |
Overview
Sema4b encodes the transmembrane guidance cue SEMA4B, a class 4 semaphorin that participates in contact-dependent signaling to regulate cell adhesion, migration, and cytoskeletal remodeling. In mouse tissues, SEMA4B contributes to axon guidance and synaptic organization and has been implicated in glial and neuronal responses to inflammatory and injury-related cues. Semaphorin signaling intersects with pathways controlling Rho-family GTPases and receptor-associated kinase cascades, shaping directional motility and tissue patterning. Dysregulated semaphorin networks, including SEMA4B-associated signaling, are studied in contexts of neurodevelopmental perturbation, neuroinflammation, and tumor–microenvironment interactions where guidance signals influence invasion and immune cell positioning.
SEMA4B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sema4b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sema4b 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 Sema4b 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 SEMA4B protein expression.
This CRISPR knockout system enables efficient generation of Sema4b-deficient cell models for investigation of SEMA4B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sema4b exon(s) critical for SEMA4B 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 Sema4b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SEMA4B CRISPR/Cas9 KO Plasmid (m) and SEMA4B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sema4b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SEMA4B HDR Plasmid (m) and SEMA4B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sema4b homology arms to support homology-directed repair at defined Sema4b 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.