Date published: 2026-7-12

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AGXT CRISPR/Cas9 KO Plasmid (m): sc-419052

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

    AGXT CRISPR/Cas9 KO Plasmid (m)

    sc-419052
    20 µg
    $397.00

    Overview

    Mouse Agxt encodes alanine–glyoxylate aminotransferase (AGXT), a peroxisomal PLP-dependent enzyme that converts glyoxylate to glycine and links amino acid catabolism to glyoxylate detoxification. This activity supports hepatic metabolic homeostasis by limiting oxalate formation and integrating peroxisomal redox and substrate flux with mitochondrial and cytosolic metabolism. Disruption of AGXT function is associated with glyoxylate accumulation and oxalate overproduction phenotypes that model pathways implicated in hyperoxaluria-like metabolic disturbances. Agxt is therefore a useful target for studying peroxisome biology, metabolite-driven oxidative stress, and genotype–metabolism relationships in mouse systems.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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