Date published: 2026-8-27

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TREX-1 CRISPR/Cas9 KO Plasmid (m): sc-423502

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TREX-1 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 TREX-1 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: TREX-1 Antibody (C-11): sc-133112
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TREX-1 CRISPR/Cas9 KO Plasmid (m)

    sc-423502
    20 µg
    $397.00

    Overview

    Trex1 encodes TREX-1, a 3′→5′ DNA exonuclease that degrades aberrant cytosolic DNA arising from endogenous retroelements, replication stress, or DNA damage, thereby limiting inappropriate activation of innate immune sensors. By restraining cGAS–STING signaling and downstream type I interferon transcriptional programs, TREX-1 helps maintain immune homeostasis and prevents chronic inflammatory responses to self nucleic acids. In mouse systems, Trex1 loss is commonly used to model nucleic acid–driven autoinflammation and to interrogate mechanisms linking genome instability, cell death pathways, and interferon-stimulated gene expression. TREX-1 activity also intersects with DNA repair and replication-associated processes, making it relevant for studies of genotoxic stress and immune surveillance.

    TREX-1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trex1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trex1 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 Trex1 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 TREX-1 protein expression.

    This CRISPR knockout system enables efficient generation of Trex1-deficient cell models for investigation of TREX-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Trex1 exon(s) critical for TREX-1 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 Trex1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TREX-1 CRISPR/Cas9 KO Plasmid (m) and TREX-1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trex1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TREX-1 HDR Plasmid (m) and TREX-1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trex1 homology arms to support homology-directed repair at defined Trex1 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.