Date published: 2026-7-21

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TDG Double Nickase Plasmid (h): sc-416599-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TDG Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
  • Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
  • One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
  • TDG Double Nickase Plasmid (h) and TDG Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TDG. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TDG Antibody (D-11): sc-376652
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TDG Double Nickase Plasmid (h)

    sc-416599-NIC
    20 µg
    $410.00

    Thymine DNA glycosylase (TDG) is a base excision repair enzyme that excises thymine or uracil from G:T and G:U mismatches arising from deamination of 5-methylcytosine, helping preserve genome integrity. Beyond canonical repair, TDG contributes to active DNA demethylation by processing oxidized 5-methylcytosine derivatives in concert with TET enzymes, linking it to epigenetic regulation of transcription. Through these activities, TDG impacts replication- and transcription-coupled repair, chromatin state, and cellular responses to DNA damage. Altered TDG function or regulation is frequently studied in the context of mutational burden, epigenome instability, and cancer-associated gene expression programs.

    TDG Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TDG locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TDG. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt TDG function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.

    To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of TDG-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.