Date published: 2026-7-9

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CEP164 CRISPR/Cas9 KO Plasmid (h): sc-403550

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CEP164 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 CEP164 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: CEP164 Antibody (E-9): sc-515403
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CEP164 CRISPR/Cas9 KO Plasmid (h)

    sc-403550
    20 µg
    $397.00

    Overview

    CEP164 (centrosomal protein 164) is a distal appendage component of the mother centriole that is required for primary cilium initiation and docking of ciliary vesicles to the basal body. It functions as a scaffold for assembly of distal appendages and supports recruitment of cilia biogenesis factors, linking centrosome maturation to ciliogenesis and cell cycle regulation. Through its role in centrosome–cilium axis control, CEP164 influences signaling pathways coordinated by primary cilia, including Hedgehog-dependent processes. Dysregulation or mutation of CEP164 is associated with ciliopathy phenotypes, notably nephronophthisis-related disorders and broader developmental abnormalities connected to impaired ciliary function.

    CEP164 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CEP164 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CEP164 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 CEP164 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 CEP164 protein expression.

    This CRISPR knockout system enables efficient generation of CEP164-deficient cell models for investigation of CEP164 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting CEP164 exon(s) critical for CEP164 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 CEP164 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CEP164 CRISPR/Cas9 KO Plasmid (h) and CEP164 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CEP164 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CEP164 HDR Plasmid (h) and CEP164 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CEP164 homology arms to support homology-directed repair at defined CEP164 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.