Date published: 2026-7-9

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ARF5 CRISPR/Cas9 KO Plasmid (m): sc-419190

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ARF5 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 ARF5 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

    ARF5 CRISPR/Cas9 KO Plasmid (m)

    sc-419190
    20 µg
    $397.00

    Overview

    Arf5 encodes ADP-ribosylation factor 5 (ARF5), a small GTPase that cycles between GDP- and GTP-bound states to regulate membrane trafficking and organelle dynamics. ARF5 coordinates vesicle budding and cargo sorting at the Golgi and endosomal membranes and contributes to COPI-dependent transport, phospholipid remodeling, and actin-associated processes through ARF effector pathways. By shaping secretory and endocytic flux, ARF5 influences receptor recycling, intracellular signaling compartmentalization, and cellular stress responses. Dysregulated ARF-family GTPase circuitry and vesicle transport programs are frequently studied in the context of aberrant proliferation, migration, and neurodevelopmental phenotypes, making Arf5 a relevant target in mechanistic disease models.

    ARF5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Arf5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Arf5 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 Arf5 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 ARF5 protein expression.

    This CRISPR knockout system enables efficient generation of Arf5-deficient cell models for investigation of ARF5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Arf5 exon(s) critical for ARF5 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 Arf5 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by ARF5 CRISPR/Cas9 KO Plasmid (m) and ARF5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Arf5 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by ARF5 HDR Plasmid (m) and ARF5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Arf5 homology arms to support homology-directed repair at defined Arf5 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.