Date published: 2026-9-5

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ADK CRISPR/Cas9 KO Plasmid (m): sc-419008

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ADK 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 ADK 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: ADK Antibody (H-1): sc-514588
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ADK CRISPR/Cas9 KO Plasmid (m)

    sc-419008
    20 µg
    $397.00

    Overview

    Mouse Adk encodes adenosine kinase (ADK), a key cytosolic enzyme that phosphorylates adenosine to AMP and helps maintain adenosine homeostasis and adenine nucleotide pools. By regulating intracellular and extracellular adenosine levels, ADK influences purinergic signaling, energy metabolism, and methylation potential through effects on the S-adenosylmethionine/S-adenosylhomocysteine cycle. ADK activity is linked to control of cellular stress responses and inflammatory signaling, and altered adenosine metabolism has been associated with neurological dysfunction, seizure susceptibility, and tissue injury contexts in experimental models. As a metabolic gatekeeper, ADK is frequently studied in pathways connecting nucleotide salvage, epigenetic regulation, and immunometabolic adaptation.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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