Date published: 2026-7-10

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ACADS CRISPR/Cas9 KO Plasmid (m): sc-418940

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ACADS 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 ACADS 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: ACADS Antibody (G-10): sc-365953
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ACADS CRISPR/Cas9 KO Plasmid (m)

    sc-418940
    20 µg
    $397.00

    Overview

    Acads encodes acyl-CoA dehydrogenase, short chain (ACADS), a mitochondrial flavoprotein that catalyzes the first dehydrogenation step in β-oxidation of short-chain fatty acids. By supporting acetyl-CoA production and downstream TCA cycle flux, ACADS helps maintain energy homeostasis during fasting and high-fat utilization, and interfaces with redox balance through FAD-dependent electron transfer. Disruption of ACADS activity is linked to short-chain acyl-CoA accumulation and altered acylcarnitine profiles, making it relevant to inborn errors of fatty acid oxidation and metabolic stress phenotypes. In mouse models, Acads is commonly studied in liver, heart, skeletal muscle, and brown adipose tissue to understand mitochondrial metabolism, nutrient sensing, and systemic energy balance.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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