Date published: 2026-7-5

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FBXO3 CRISPR/Cas9 KO Plasmid (m): sc-425412

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FBXO3 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 FBXO3 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: FBXO3 Antibody (C-7): sc-514625
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FBXO3 CRISPR/Cas9 KO Plasmid (m)

    sc-425412
    20 µg
    $397.00

    Overview

    Fbxo3 encodes the F-box protein FBXO3 in mouse, a substrate-recognition component of SCF (SKP1–CUL1–RBX1) E3 ubiquitin ligase complexes that help control proteostasis through ubiquitin-dependent protein turnover. By directing selective ubiquitination, FBXO3 influences cell signaling dynamics, cell-cycle and stress-response programs, and the stability of pathway regulators. Altered activity within SCF–F-box networks has been associated with dysregulated inflammation and broader immune signaling, as well as changes in cellular homeostasis relevant to disease biology. These features make Fbxo3 a useful node for studying ubiquitin–proteasome pathway control of signaling and phenotype.

    FBXO3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fbxo3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fbxo3 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 Fbxo3 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 FBXO3 protein expression.

    This CRISPR knockout system enables efficient generation of Fbxo3-deficient cell models for investigation of FBXO3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Fbxo3 exon(s) critical for FBXO3 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 Fbxo3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by FBXO3 CRISPR/Cas9 KO Plasmid (m) and FBXO3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fbxo3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by FBXO3 HDR Plasmid (m) and FBXO3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fbxo3 homology arms to support homology-directed repair at defined Fbxo3 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.