Date published: 2026-8-4

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MCT9 Double Nickase Plasmid (h): sc-409073-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • MCT9 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
  • MCT9 Double Nickase Plasmid (h) and MCT9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC16A9. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    MCT9 Double Nickase Plasmid (h)

    sc-409073-NIC
    20 µg
    $410.00

    MCT9 Double Nickase Plasmid (h2)

    sc-409073-NIC-2
    20 µg
    $410.00

    SLC16A9 encodes monocarboxylate transporter 9 (MCT9), a member of the SLC16 family implicated in transmembrane flux of small organic acids and related metabolites that influence cellular energy balance. By shaping intracellular and extracellular metabolite availability, MCT9 can intersect with pathways governing metabolic homeostasis and transport-coupled signaling. Genetic variation and dysregulated expression of SLC16A9 have been associated with altered urate handling and broader metabolic phenotypes, supporting its relevance in studies of renal transport biology and systemic metabolite regulation. As a transporter-linked node in metabolic networks, MCT9 is frequently examined in contexts such as nutrient sensing, redox balance, and transporter–enzyme coupling.

    MCT9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC16A9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC16A9. 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 SLC16A9 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 SLC16A9-disrupted clones.

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