Date published: 2026-7-15

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Vav CRISPR/Cas9 KO Plasmid (m): sc-423655

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Vav 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 Vav 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: Vav Antibody (D-7): sc-8039
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Vav CRISPR/Cas9 KO Plasmid (m)

    sc-423655
    20 µg
    $397.00

    Overview

    Vav1 encodes Vav, a hematopoietic-specific guanine nucleotide exchange factor that activates Rho family GTPases such as Rac1 and Cdc42 to coordinate cytoskeletal remodeling and signal propagation. In mouse immune cells, Vav1 integrates signaling downstream of antigen receptors and Fc receptors, linking tyrosine kinase pathways to MAPK, NF-κB, and calcium-dependent transcriptional programs. These activities shape T cell development, activation, and migration, and influence antigen-driven effector functions across lymphoid lineages. Dysregulated Vav1 signaling has been associated with immune dysfunction and oncogenic signaling contexts in hematologic disease models, making it a key node for mechanistic studies of leukocyte signaling networks.

    Vav CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Vav1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Vav1 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 Vav1 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 Vav protein expression.

    This CRISPR knockout system enables efficient generation of Vav1-deficient cell models for investigation of Vav signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Vav1 exon(s) critical for Vav 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 Vav1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Vav CRISPR/Cas9 KO Plasmid (m) and Vav CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Vav1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Vav HDR Plasmid (m) and Vav HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Vav1 homology arms to support homology-directed repair at defined Vav1 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.