Date published: 2026-7-6

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Cdc7 CRISPR/Cas9 KO Plasmid (m): sc-419586

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Cdc7 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 Cdc7 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

    Cdc7 CRISPR/Cas9 KO Plasmid (m)

    sc-419586
    20 µg
    $397.00

    Overview

    Cdc7 (cell division cycle 7) encodes a serine/threonine kinase that functions as the catalytic subunit of the DDK complex, a core regulator of DNA replication initiation. Cdc7 phosphorylates MCM helicase components to promote origin firing and coordinate S-phase progression with checkpoint control, integrating signals from replication stress pathways. Through its roles in genome duplication and replication fork stability, Cdc7 activity influences chromosomal integrity and cell-cycle dynamics in proliferative tissues. Dysregulated Cdc7 signaling has been linked to aberrant proliferation and genomic instability phenotypes that are frequently interrogated in cancer biology and DNA damage response research.

    Cdc7 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cdc7 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cdc7 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 Cdc7 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 Cdc7 protein expression.

    This CRISPR knockout system enables efficient generation of Cdc7-deficient cell models for investigation of Cdc7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Cdc7 exon(s) critical for Cdc7 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 Cdc7 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Cdc7 CRISPR/Cas9 KO Plasmid (m) and Cdc7 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cdc7 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Cdc7 HDR Plasmid (m) and Cdc7 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cdc7 homology arms to support homology-directed repair at defined Cdc7 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.