Date published: 2026-7-9

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apoB CRISPR/Cas9 KO Plasmid (m): sc-433607

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • apoB 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 apoB 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: apoB Antibody (A-6): sc-393636
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    apoB CRISPR/Cas9 KO Plasmid (m)

    sc-433607
    20 µg
    $397.00

    Overview

    Mouse Apob encodes apolipoprotein B (apoB), the essential structural apolipoprotein required for assembly and secretion of triglyceride-rich lipoproteins, including chylomicrons and VLDL, and for subsequent formation of LDL. ApoB coordinates lipoprotein biogenesis in the endoplasmic reticulum through interactions with microsomal triglyceride transfer protein, linking hepatic and intestinal lipid handling to systemic cholesterol transport. By governing particle number and composition, apoB influences lipoprotein receptor engagement, lipid uptake, and downstream metabolic signaling. Dysregulation of APOB-dependent pathways is widely used to model hyperlipidemia, fatty liver phenotypes, and atherosclerosis-relevant lipid trafficking in mice.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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