Date published: 2026-9-3

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SLC25A20 Double Nickase Plasmid (h): sc-407585-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SLC25A20 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
  • SLC25A20 Double Nickase Plasmid (h) and SLC25A20 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SLC25A20. One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SLC25A20 Double Nickase Plasmid (h)

    sc-407585-NIC
    20 µg
    $410.00

    SLC25A20 Double Nickase Plasmid (h2)

    sc-407585-NIC-2
    20 µg
    $410.00

    SLC25A20 encodes carnitine–acylcarnitine translocase (CACT), an inner mitochondrial membrane carrier that exchanges acylcarnitines for free carnitine to enable import of long-chain fatty acids for β-oxidation. This transport step links the carnitine shuttle to mitochondrial energy metabolism and supports ATP production from lipid substrates, particularly in high-energy tissues. Disruption of SLC25A20 perturbs fatty acid oxidation and can alter acylcarnitine profiles, redox balance, and downstream metabolic signaling. Variants in SLC25A20 are associated with inborn errors of metabolism involving impaired long-chain fatty acid utilization, making it a useful target for studying mitochondrial transport, metabolic stress responses, and lipid catabolism networks.

    SLC25A20 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SLC25A20 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SLC25A20. 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 SLC25A20 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 SLC25A20-disrupted clones.

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