Date published: 2026-7-14

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TrxR2 Double Nickase Plasmid (h): sc-402671-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TrxR2 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
  • TrxR2 Double Nickase Plasmid (h) and TrxR2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TXNRD2. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TrxR2 Antibody (B-10): sc-365714
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TrxR2 Double Nickase Plasmid (h)

    sc-402671-NIC
    20 µg
    $410.00

    TrxR2 Double Nickase Plasmid (h2)

    sc-402671-NIC-2
    20 µg
    $410.00

    TXNRD2 encodes human mitochondrial thioredoxin reductase 2 (TrxR2), a selenoenzyme that uses NADPH to maintain thioredoxin-2 in a reduced state and preserve mitochondrial redox homeostasis. Through control of thiol–disulfide exchange, TrxR2 supports antioxidant defense, protein folding quality control, and redox-sensitive signaling that influence mitochondrial metabolism and apoptosis. TXNRD2 activity interfaces with ROS handling and mitochondrial stress responses, shaping cellular adaptation to oxidative challenges. Dysregulation of mitochondrial thioredoxin systems is frequently examined in contexts of metabolic imbalance, neurodegeneration, and cancer-associated redox remodeling.

    TrxR2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TXNRD2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TXNRD2. 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 TXNRD2 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 TXNRD2-disrupted clones.

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