Date published: 2026-7-9

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SLC39A13 CRISPR/Cas9 KO Plasmid (h): sc-406673

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SLC39A13 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 SLC39A13 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

    SLC39A13 CRISPR/Cas9 KO Plasmid (h)

    sc-406673
    20 µg
    $397.00

    Overview

    SLC39A13 (ZIP13) is a member of the SLC39 zinc importer family that regulates intracellular Zn2+ distribution by transporting zinc from intracellular compartments into the cytosol. By shaping zinc availability, SLC39A13 influences metalloprotein activity, redox homeostasis, and signaling pathways that depend on zinc as a structural or catalytic cofactor, including processes linked to extracellular matrix organization and connective tissue development. Genetic disruption of SLC39A13 has been associated with a spondylocheiro dysplastic form of Ehlers–Danlos syndrome, highlighting its relevance to collagen maturation, tissue integrity, and mechanobiology. Altered zinc transport mediated by ZIP13 has also been connected to dysregulated fibroblast function and broad transcriptional responses to metal stress.

    SLC39A13 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SLC39A13 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SLC39A13 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 SLC39A13 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 SLC39A13 protein expression.

    This CRISPR knockout system enables efficient generation of SLC39A13-deficient cell models for investigation of SLC39A13 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting SLC39A13 exon(s) critical for SLC39A13 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 SLC39A13 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by SLC39A13 CRISPR/Cas9 KO Plasmid (h) and SLC39A13 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SLC39A13 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by SLC39A13 HDR Plasmid (h) and SLC39A13 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SLC39A13 homology arms to support homology-directed repair at defined SLC39A13 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.