Date published: 2026-9-10

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DHRS1 Double Nickase Plasmid (h): sc-414077-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • DHRS1 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
  • DHRS1 Double Nickase Plasmid (h) and DHRS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DHRS1. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    DHRS1 Double Nickase Plasmid (h)

    sc-414077-NIC
    20 µg
    $410.00

    DHRS1 (dehydrogenase/reductase 1) encodes a cytosolic short-chain dehydrogenase/reductase that catalyzes NAD(P)H-dependent redox reactions, contributing to cellular carbonyl metabolism and maintenance of redox balance. By modulating interconversion of aldehydes, ketones, and related lipid- and steroid-derived metabolites, DHRS1 can influence metabolic homeostasis and responses to oxidative stress. Altered expression or activity of SDR enzymes has been linked to dysregulated lipid metabolism and redox signaling in human disease contexts, including cancer-associated metabolic reprogramming. DHRS1 is therefore studied in pathways connecting oxidative stress, mitochondrial function, and metabolite-driven regulation of cell growth and differentiation.

    DHRS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DHRS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DHRS1. 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 DHRS1 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 DHRS1-disrupted clones.

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