Date published: 2026-8-22

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USP30 Double Nickase Plasmid (h): sc-407851-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • USP30 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
  • USP30 Double Nickase Plasmid (h) and USP30 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting USP30. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: USP30 Antibody (B-6): sc-515235
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    USP30 Double Nickase Plasmid (h)

    sc-407851-NIC
    20 µg
    $410.00

    USP30 Double Nickase Plasmid (h2)

    sc-407851-NIC-2
    20 µg
    $410.00

    Human USP30 encodes a mitochondrial outer membrane deubiquitinase that counterbalances ubiquitin-dependent signaling on damaged mitochondria. By removing ubiquitin chains from substrates labeled by PINK1/Parkin, USP30 modulates mitophagy initiation, mitochondrial protein turnover, and organelle quality control. This activity intersects with ubiquitin–proteasome and autophagy-lysosome pathways, influencing mitochondrial dynamics and cellular stress responses. Dysregulated USP30-linked ubiquitination has been implicated in mechanisms relevant to neurodegeneration and other disorders characterized by impaired mitochondrial homeostasis.

    USP30 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the USP30 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within USP30. 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 USP30 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 USP30-disrupted clones.

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