Date published: 2026-7-10

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NOXA Double Nickase Plasmid (h): sc-400498-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • NOXA 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
  • NOXA Double Nickase Plasmid (h) and NOXA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PMAIP1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: NOXA Antibody (F-3): sc-515840
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    NOXA Double Nickase Plasmid (h)

    sc-400498-NIC
    20 µg
    $410.00

    PMAIP1 encodes the BH3-only protein NOXA, a p53-responsive pro-apoptotic regulator that promotes mitochondrial outer membrane permeabilization by neutralizing anti-apoptotic BCL2 family members, with strong selectivity for MCL1 and BCL2A1. NOXA integrates DNA damage and oncogenic stress signals to engage the intrinsic apoptosis pathway, influencing caspase activation, cellular fitness, and stress-induced cell fate decisions. Its expression and turnover are further shaped by ubiquitin-mediated proteostasis and transcriptional programs downstream of p53 and related stress pathways. Dysregulation of the PMAIP1–NOXA axis is frequently studied in contexts of altered apoptosis sensitivity, including cancer biology and mechanisms of resistance to mitochondrial apoptosis.

    NOXA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PMAIP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PMAIP1. 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 PMAIP1 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 PMAIP1-disrupted clones.

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