SEMA6A CRISPR/Cas9 KO Plasmid (m): sc-422887
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA6A 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 SEMA6A 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: SEMA6A Antibody (B-3): sc-398302
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SEMA6A CRISPR/Cas9 KO Plasmid (m) | sc-422887 | 20 µg | $397.00 |
Overview
Sema6a encodes the transmembrane guidance cue SEMA6A, a class 6 semaphorin that shapes neural circuit assembly by regulating growth cone behavior, axon pathfinding, and neuronal migration. Through interactions with plexin receptors and downstream Rho family GTPase signaling, SEMA6A influences cytoskeletal dynamics, cell adhesion, and contact-mediated repulsion during development. In mouse models, altered Sema6a function has been linked to defects in thalamocortical and corticospinal connectivity and broader neurodevelopmental phenotypes, supporting its relevance to mechanisms underlying neural wiring disorders. SEMA6A-dependent signaling is also studied in contexts where semaphorin pathways modulate cell motility and tissue patterning.
SEMA6A CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sema6a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sema6a 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 Sema6a 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 SEMA6A protein expression.
This CRISPR knockout system enables efficient generation of Sema6a-deficient cell models for investigation of SEMA6A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sema6a exon(s) critical for SEMA6A 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 Sema6a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SEMA6A CRISPR/Cas9 KO Plasmid (m) and SEMA6A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sema6a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SEMA6A HDR Plasmid (m) and SEMA6A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sema6a homology arms to support homology-directed repair at defined Sema6a 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.