Date published: 2026-8-30

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ZAG CRISPR/Cas9 KO Plasmid (m): sc-419279

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ZAG 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 ZAG 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: ZAG Antibody (F-6): sc-271957
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ZAG CRISPR/Cas9 KO Plasmid (m)

    sc-419279
    20 µg
    $397.00

    Overview

    Azgp1 encodes zinc-α2-glycoprotein (ZAG), a secreted adipokine-like glycoprotein expressed in multiple tissues that contributes to systemic lipid mobilization and energy balance. In mouse metabolic networks, ZAG has been linked to regulation of adipocyte lipolysis, modulation of fatty acid utilization, and cross-talk with inflammatory signaling in adipose and liver microenvironments. Altered Azgp1/ZAG expression is frequently studied in the context of obesity-associated metabolic dysfunction and changes in insulin sensitivity, as well as broader cachexia- and inflammation-related phenotypes. As a circulating and extracellular matrix-associated factor, ZAG is also relevant to investigations of tissue remodeling and intercellular communication.

    ZAG CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Azgp1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Azgp1 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 Azgp1 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 ZAG protein expression.

    This CRISPR knockout system enables efficient generation of Azgp1-deficient cell models for investigation of ZAG signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Azgp1 exon(s) critical for ZAG 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 Azgp1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by ZAG CRISPR/Cas9 KO Plasmid (m) and ZAG CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Azgp1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by ZAG HDR Plasmid (m) and ZAG HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Azgp1 homology arms to support homology-directed repair at defined Azgp1 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.