Date published: 2026-9-17

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CUZD1 CRISPR/Cas9 KO Plasmid (h): sc-407311

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CUZD1 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 CUZD1 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: CUZD1 Antibody (E-10): sc-514578
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CUZD1 CRISPR/Cas9 KO Plasmid (h)

    sc-407311
    20 µg
    $397.00

    Overview

    CUZD1 (CUB and zona pellucida-like domains 1) encodes a secreted and membrane-associated protein implicated in epithelial cell differentiation and secretory tissue homeostasis. CUZD1 participates in processes linked to protein trafficking and regulated secretion and has been connected to transcriptional programs downstream of cytokine signaling, including pathways associated with JAK/STAT activity in glandular epithelia. Altered CUZD1 expression has been reported in epithelial-derived malignancies and inflammatory states, supporting its use as a molecular node for studying cell state transitions, stress responses, and tumor-associated phenotypes. In human model systems, CUZD1 provides a tractable target for dissecting mechanisms of epithelial remodeling and context-dependent signaling outputs.

    CUZD1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CUZD1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CUZD1 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 CUZD1 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 CUZD1 protein expression.

    This CRISPR knockout system enables efficient generation of CUZD1-deficient cell models for investigation of CUZD1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting CUZD1 exon(s) critical for CUZD1 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 CUZD1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CUZD1 CRISPR/Cas9 KO Plasmid (h) and CUZD1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CUZD1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CUZD1 HDR Plasmid (h) and CUZD1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CUZD1 homology arms to support homology-directed repair at defined CUZD1 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.