Date published: 2026-10-9

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VEGF-C CRISPR/Cas9 KO Plasmid (m): sc-423667

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • VEGF-C 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 VEGF-C 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: VEGF-C Antibody (E-6): sc-374628
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    VEGF-C CRISPR/Cas9 KO Plasmid (m)

    sc-423667
    20 µg
    $397.00

    Overview

    Vegfc encodes vascular endothelial growth factor C (VEGF-C), a secreted ligand that regulates lymphangiogenesis and vascular remodeling primarily through activation of VEGFR3/FLT4 and, in some contexts, VEGFR2/KDR. VEGF-C signaling engages downstream MAPK/ERK and PI3K–AKT pathways to influence endothelial cell proliferation, migration, and survival, shaping lymphatic vessel development and tissue fluid homeostasis. In mouse models, altered Vegfc activity is widely used to study mechanisms of lymphatic dysfunction, inflammatory edema, and tumor-associated lymphangiogenesis, as well as lymphatic contributions to immune cell trafficking.

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

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

    Key Features

    • sgRNAs targeting Vegfc exon(s) critical for VEGF-C 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 Vegfc genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

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