Date published: 2026-7-9

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SEMA3E CRISPR/Cas9 KO Plasmid (m): sc-422878

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SEMA3E 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 SEMA3E 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SEMA3E CRISPR/Cas9 KO Plasmid (m)

    sc-422878
    20 µg
    $397.00

    Overview

    Mouse Sema3e encodes semaphorin-3E (SEMA3E), a secreted guidance cue that signals primarily through plexin receptors to control axon pathfinding, neuronal migration, and tissue patterning. SEMA3E modulates cytoskeletal dynamics and cell adhesion, intersecting with pathways governing motility, angiogenic remodeling, and immune cell trafficking in a context-dependent manner. Dysregulated SEMA3E–plexin signaling has been linked in the literature to aberrant vascular development and altered invasive behavior in cancer biology models, supporting its relevance to studies of neurodevelopment and microenvironmental signaling.

    SEMA3E CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Sema3e gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Sema3e 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 Sema3e 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 SEMA3E protein expression.

    This CRISPR knockout system enables efficient generation of Sema3e-deficient cell models for investigation of SEMA3E signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Sema3e exon(s) critical for SEMA3E 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 Sema3e genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SEMA3E CRISPR/Cas9 KO Plasmid (m) and SEMA3E CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Sema3e locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SEMA3E HDR Plasmid (m) and SEMA3E HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Sema3e homology arms to support homology-directed repair at defined Sema3e 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.