Date published: 2026-7-15

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MAFbx CRISPR/Cas9 KO Plasmid (h): sc-400908

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

    MAFbx CRISPR/Cas9 KO Plasmid (h)

    sc-400908
    20 µg
    $397.00

    Overview

    FBXO32 encodes the human muscle atrophy F-box protein MAFbx (also known as Atrogin-1), an SCF (SKP1–CUL1–F-box) E3 ubiquitin ligase component that confers substrate specificity for ubiquitin-dependent proteasomal degradation. MAFbx is strongly induced during catabolic states and contributes to proteostasis remodeling by targeting regulators of muscle differentiation and growth, linking it to pathways downstream of FOXO transcription factors, IGF-1/AKT signaling, and cellular stress responses. Through its role in ubiquitin–proteasome system activity, FBXO32 is widely studied in muscle wasting and remodeling contexts, including cachexia-associated atrophy and disuse-related muscle loss. Altered FBXO32/MAFbx activity is also relevant for understanding skeletal muscle adaptation, metabolic stress, and inflammatory signaling inputs that converge on protein turnover.

    MAFbx CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FBXO32 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FBXO32 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 FBXO32 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 MAFbx protein expression.

    This CRISPR knockout system enables efficient generation of FBXO32-deficient cell models for investigation of MAFbx signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting FBXO32 exon(s) critical for MAFbx 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 FBXO32 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by MAFbx CRISPR/Cas9 KO Plasmid (h) and MAFbx CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FBXO32 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by MAFbx HDR Plasmid (h) and MAFbx HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FBXO32 homology arms to support homology-directed repair at defined FBXO32 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.