Date published: 2026-7-10

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PRAT4A CRISPR/Cas9 KO Plasmid (h): sc-404775

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • PRAT4A 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 PRAT4A 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: PRAT4A Antibody (F-6): sc-515151
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    PRAT4A CRISPR/Cas9 KO Plasmid (h)

    sc-404775
    20 µg
    $397.00

    Overview

    CNPY3 encodes PRAT4A, an endoplasmic reticulum–resident co-chaperone that supports maturation and quality control of Toll-like receptors (TLRs) and related innate immune receptors. PRAT4A participates in early secretory pathway processes that govern receptor folding, glycosylation, and trafficking to endosomes or the plasma membrane, thereby influencing NF-κB and IRF-driven inflammatory signaling. Altered PRAT4A function can perturb pattern-recognition receptor responsiveness and cytokine programs, linking CNPY3 biology to studies of infection, inflammation, and immune dysregulation. Its role in receptor biogenesis also makes it relevant for dissecting ER proteostasis networks and cell-type-specific innate signaling states.

    PRAT4A CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CNPY3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CNPY3 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 CNPY3 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 PRAT4A protein expression.

    This CRISPR knockout system enables efficient generation of CNPY3-deficient cell models for investigation of PRAT4A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting CNPY3 exon(s) critical for PRAT4A 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 CNPY3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by PRAT4A CRISPR/Cas9 KO Plasmid (h) and PRAT4A CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CNPY3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by PRAT4A HDR Plasmid (h) and PRAT4A HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CNPY3 homology arms to support homology-directed repair at defined CNPY3 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.