Date published: 2026-9-22

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TDO2 CRISPR/Cas9 KO Plasmid (h): sc-402482

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TDO2 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 TDO2 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

    TDO2 CRISPR/Cas9 KO Plasmid (h)

    sc-402482
    20 µg
    $397.00

    Overview

    TDO2 (tryptophan 2,3-dioxygenase) is a heme-dependent enzyme that catalyzes the first and rate-limiting step of tryptophan degradation through the kynurenine pathway, converting L-tryptophan to N-formylkynurenine. By controlling intracellular tryptophan availability and downstream kynurenine metabolites, TDO2 influences cellular metabolic homeostasis and can modulate signaling through pathways responsive to amino acid depletion and metabolite-driven transcriptional programs, including aryl hydrocarbon receptor (AHR) activity. TDO2 expression is most prominent in liver but is also studied in extrahepatic contexts where altered tryptophan catabolism impacts redox balance, NAD+ precursor flux, and immune-metabolic crosstalk. Dysregulated kynurenine pathway activity involving TDO2 has been associated with inflammation and cancer-related metabolic remodeling, supporting its relevance for mechanistic studies of tumor microenvironment and immunometabolism.

    TDO2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TDO2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TDO2 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 TDO2 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 TDO2 protein expression.

    This CRISPR knockout system enables efficient generation of TDO2-deficient cell models for investigation of TDO2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting TDO2 exon(s) critical for TDO2 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 TDO2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TDO2 CRISPR/Cas9 KO Plasmid (h) and TDO2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TDO2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TDO2 HDR Plasmid (h) and TDO2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TDO2 homology arms to support homology-directed repair at defined TDO2 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.