plexin-A3 CRISPR/Cas9 KO Plasmid (m): sc-422320
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- plexin-A3 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 plexin-A3 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 | |
plexin-A3 CRISPR/Cas9 KO Plasmid (m) | sc-422320 | 20 µg | $397.00 |
Overview
Plxna3 encodes plexin-A3, a transmembrane receptor for class 3 semaphorins that regulates axon guidance, neuronal migration, and dendritic patterning through semaphorin–neuropilin–plexin signaling. Plexin-A3 integrates cues that remodel the actin and microtubule cytoskeleton via Rho family GTPases and associated effectors, influencing growth cone collapse and directional motility. Beyond the nervous system, plexin-A3 has been linked to control of cell adhesion and movement, processes relevant to developmental patterning and tissue organization. Dysregulation of semaphorin/plexin pathways has been associated with neurodevelopmental abnormalities and altered migratory phenotypes in disease-relevant models.
plexin-A3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Plxna3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Plxna3 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 Plxna3 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 plexin-A3 protein expression.
This CRISPR knockout system enables efficient generation of Plxna3-deficient cell models for investigation of plexin-A3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Plxna3 exon(s) critical for plexin-A3 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 Plxna3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by plexin-A3 CRISPR/Cas9 KO Plasmid (m) and plexin-A3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Plxna3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by plexin-A3 HDR Plasmid (m) and plexin-A3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Plxna3 homology arms to support homology-directed repair at defined Plxna3 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.