SEMA3G CRISPR/Cas9 KO Plasmid (h): sc-406077
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA3G CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 SEMA3G 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 | |
SEMA3G CRISPR/Cas9 KO Plasmid (h) | sc-406077 | 20 µg | $397.00 |
Overview
SEMA3G encodes semaphorin-3G, a secreted guidance cue that signals through neuropilin/plexin receptor complexes to regulate cytoskeletal remodeling, cell migration, and tissue patterning. In addition to roles in axon guidance and neurodevelopment, SEMA3G influences angiogenic and lymphatic sprouting and can modulate endothelial and immune cell behavior through semaphorin-dependent signaling. These processes intersect with pathways controlling adhesion, motility, and vascular remodeling, making SEMA3G a relevant node for studying developmental biology and microenvironment-driven regulation of cell movement. Altered semaphorin signaling has been associated with cancer progression and metastasis-related phenotypes, as well as vascular and inflammatory dysfunction, supporting investigation of SEMA3G in disease-relevant models.
SEMA3G CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SEMA3G gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SEMA3G 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 SEMA3G 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 SEMA3G protein expression.
This CRISPR knockout system enables efficient generation of SEMA3G-deficient cell models for investigation of SEMA3G signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SEMA3G exon(s) critical for SEMA3G 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 SEMA3G genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SEMA3G CRISPR/Cas9 KO Plasmid (h) and SEMA3G CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SEMA3G locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SEMA3G HDR Plasmid (h) and SEMA3G HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SEMA3G homology arms to support homology-directed repair at defined SEMA3G 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.