Date published: 2026-8-25

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SIRT5 Double Nickase Plasmid (r): sc-437317-NIC

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Datasheets
  • Target species: rat
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SIRT5 Double Nickase Plasmid (r) 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
  • SIRT5 Double Nickase Plasmid (r) and SIRT5 Double Nickase Plasmid (r2) encode distinct paired gRNA designs targeting . One or both designs may be available
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SIRT5 Double Nickase Plasmid (r)

    sc-437317-NIC
    20 µg
    $410.00

    SIRT5 Double Nickase Plasmid (r2)

    sc-437317-NIC-2
    20 µg
    $410.00

    SIRT5 is a mitochondrial NAD+-dependent lysine deacylase within the sirtuin family that preferentially removes succinyl, malonyl, and glutaryl modifications from metabolic enzymes. By regulating acylation state, SIRT5 influences central carbon metabolism, including the urea cycle, fatty acid oxidation, TCA-cycle flux, and oxidative stress responses through modulation of mitochondrial enzyme activity. In rat systems, altered SIRT5 function is used to probe links between mitochondrial proteostasis and bioenergetic reprogramming in conditions associated with metabolic stress and tissue injury. These pathways are frequently interrogated in models of liver metabolism, cardiac energetics, and neuroinflammation where post-translational acylation dynamics can impact cellular resilience.

    SIRT5 Double Nickase Plasmid (r) consists of a matched pair of plasmids engineered for high-specificity editing of the locus in rat cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within . 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 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 -disrupted clones.

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