Date published: 2026-8-12

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CUL-4A CRISPR/Cas9 KO Plasmid (m): sc-430261

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CUL-4A 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 CUL-4A 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

    CUL-4A CRISPR/Cas9 KO Plasmid (m)

    sc-430261
    20 µg
    $397.00

    Overview

    Mouse Cul4a encodes CUL-4A, a cullin scaffold protein that assembles CUL4–DDB1 E3 ubiquitin ligase complexes to direct ubiquitination and proteasomal turnover of key regulators of chromatin dynamics and genome stability. CUL-4A participates in DNA damage recognition and repair signaling, including nucleotide excision repair and replication-associated processes, and helps coordinate cell-cycle progression through regulated protein degradation. By shaping proteostasis at chromatin, CUL-4A influences transcriptional programs and checkpoint responses under genotoxic stress. Dysregulated CUL4A-dependent ubiquitination has been linked to aberrant proliferation and genomic instability phenotypes, making Cul4a a useful target for mechanistic studies of oncogenic pathways in mouse models.

    CUL-4A CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cul4a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cul4a 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 Cul4a 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 CUL-4A protein expression.

    This CRISPR knockout system enables efficient generation of Cul4a-deficient cell models for investigation of CUL-4A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Cul4a exon(s) critical for CUL-4A 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 Cul4a genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CUL-4A CRISPR/Cas9 KO Plasmid (m) and CUL-4A CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cul4a locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CUL-4A HDR Plasmid (m) and CUL-4A HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cul4a homology arms to support homology-directed repair at defined Cul4a 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.