SEMA6B CRISPR/Cas9 KO Plasmid (m): sc-422888
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA6B 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 SEMA6B 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: SEMA6B Antibody (G-7): sc-390928
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SEMA6B CRISPR/Cas9 KO Plasmid (m) | sc-422888 | 20 µg | $397.00 |
Overview
Sema6b encodes semaphorin-6B (SEMA6B), a transmembrane guidance cue that signals through plexin family receptors to regulate cell–cell communication, cytoskeletal remodeling, and directional migration. In the nervous system it contributes to axon guidance, neurite outgrowth, and synaptic organization, integrating with Rho GTPase- and kinase-dependent pathways that shape growth cone dynamics and tissue patterning. Beyond neurodevelopment, semaphorin signaling influences immune cell positioning and vascular remodeling, linking SEMA6B-dependent processes to inflammation- and angiogenesis-associated phenotypes. Altered semaphorin–plexin signaling has been implicated in developmental abnormalities and dysregulated cell motility programs relevant to neurological and oncogenic contexts, providing a rationale for mechanistic studies in mouse models.
SEMA6B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sema6b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sema6b 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 Sema6b 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 SEMA6B protein expression.
This CRISPR knockout system enables efficient generation of Sema6b-deficient cell models for investigation of SEMA6B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Sema6b exon(s) critical for SEMA6B 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 Sema6b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SEMA6B CRISPR/Cas9 KO Plasmid (m) and SEMA6B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sema6b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SEMA6B HDR Plasmid (m) and SEMA6B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sema6b homology arms to support homology-directed repair at defined Sema6b 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.