Date published: 2026-8-29

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SNX5 CRISPR/Cas9 KO Plasmid (h): sc-404660

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SNX5 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 SNX5 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: SNX5 Antibody (F-11): sc-515215
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SNX5 CRISPR/Cas9 KO Plasmid (h)

    sc-404660
    20 µg
    $397.00

    Overview

    Human SNX5 (sorting nexin 5) encodes a PX domain–containing endosomal protein that binds phosphoinositides and cooperates with membrane remodeling factors to regulate cargo sorting and vesicular trafficking. SNX5 participates in endosome-to-Golgi and endosomal recycling routes, supporting receptor turnover and signal attenuation by controlling the subcellular localization of transmembrane proteins. Through its roles in endosomal tubulation and protein complex assembly, SNX5 influences cellular homeostasis processes linked to receptor-mediated signaling, nutrient uptake, and membrane composition. Altered endosomal trafficking pathways involving sorting nexins are associated with dysregulated growth factor signaling and cellular stress responses, making SNX5 relevant to mechanistic studies of disease-associated trafficking defects.

    SNX5 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SNX5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SNX5 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 SNX5 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 SNX5 protein expression.

    This CRISPR knockout system enables efficient generation of SNX5-deficient cell models for investigation of SNX5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting SNX5 exon(s) critical for SNX5 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 SNX5 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SNX5 CRISPR/Cas9 KO Plasmid (h) and SNX5 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SNX5 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SNX5 HDR Plasmid (h) and SNX5 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SNX5 homology arms to support homology-directed repair at defined SNX5 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.