Date published: 2026-8-28

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VAT1 CRISPR/Cas9 KO Plasmid (h): sc-405997

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • VAT1 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 VAT1 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: VAT1 Antibody (E-7): sc-515705
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    VAT1 CRISPR/Cas9 KO Plasmid (h)

    sc-405997
    20 µg
    $397.00

    Overview

    VAT1 (vesicle amine transport 1) encodes a conserved peripheral membrane protein enriched in neuronal and secretory tissues, where it associates with synaptic and dense-core vesicles. VAT1 has been linked to vesicle biogenesis and trafficking, supporting regulated exocytosis and endocytosis processes that shape neurotransmitter and hormone release. Through these roles, VAT1 connects to pathways governing membrane dynamics, redox-associated protein interactions, and cellular stress responses in highly secretory cells. Altered VAT1 expression has been reported in studies of neurodegeneration, cancer-associated phenotypes, and metabolic dysregulation, making it a useful node for mechanistic interrogation of vesicle-dependent signaling.

    VAT1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the VAT1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the VAT1 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 VAT1 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 VAT1 protein expression.

    This CRISPR knockout system enables efficient generation of VAT1-deficient cell models for investigation of VAT1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting VAT1 exon(s) critical for VAT1 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 VAT1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by VAT1 CRISPR/Cas9 KO Plasmid (h) and VAT1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the VAT1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by VAT1 HDR Plasmid (h) and VAT1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by VAT1 homology arms to support homology-directed repair at defined VAT1 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.