Date published: 2026-7-14

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Nek7 CRISPR/Cas9 KO Plasmid (m): sc-425603

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Nek7 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 Nek7 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: Nek7 Antibody (B-5): sc-393539
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Nek7 CRISPR/Cas9 KO Plasmid (m)

    sc-425603
    20 µg
    $397.00

    Overview

    Nek7 (NIMA-related kinase 7) is a serine/threonine kinase that functions as a key regulator of mitotic progression, coordinating centrosome activity, spindle assembly, and faithful chromosome segregation. In proliferating cells, Nek7 signaling supports cell-cycle transitions and microtubule dynamics, linking kinase control to cytoskeletal organization and checkpoints that maintain genomic stability. Nek7 has also been implicated in innate immune signaling through regulation of NLRP3 inflammasome activation, connecting cell-cycle kinases to inflammatory pathway outputs. Dysregulated Nek7 activity or expression is therefore relevant to studies of aberrant proliferation, chromosomal instability, and inflammation-associated phenotypes in mouse model systems.

    Nek7 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Nek7 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Nek7 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 Nek7 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 Nek7 protein expression.

    This CRISPR knockout system enables efficient generation of Nek7-deficient cell models for investigation of Nek7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Nek7 exon(s) critical for Nek7 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 Nek7 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Nek7 CRISPR/Cas9 KO Plasmid (m) and Nek7 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Nek7 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Nek7 HDR Plasmid (m) and Nek7 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Nek7 homology arms to support homology-directed repair at defined Nek7 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.