Date published: 2026-7-5

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p73 Double Nickase Plasmid (m2): sc-423511-NIC-2

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • p73 Double Nickase Plasmid (m2) 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
  • p73 Double Nickase Plasmid (m2) and p73 Double Nickase Plasmid (m22) encode distinct paired gRNA designs targeting Trp73. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: p73 Antibody (5B429): sc-56191
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    p73 Double Nickase Plasmid (m2)

    sc-423511-NIC-2
    20 µg
    $410.00

    The mouse Trp73 gene encodes p73, a p53-family transcription factor that regulates programs controlling cell-cycle arrest, apoptosis, and genomic stability through context-dependent activation of target genes involved in DNA damage responses. p73 also contributes to developmental processes, including neurogenesis and epithelial differentiation, and interfaces with signaling networks such as E2F-driven transcription, TGF-β–associated regulation, and stress-activated kinase pathways. Dysregulation of Trp73 isoform balance and p73-mediated transcription has been linked to altered tumor suppressor functions, chromosomal instability, and defects in tissue homeostasis that are relevant to cancer biology and developmental phenotypes. Gene editing of Trp73 in mouse models supports mechanistic studies of isoform-specific function, transcriptional circuitry, and pathway interactions underlying stress responses and disease-associated cellular states.

    p73 Double Nickase Plasmid (m2) consists of a matched pair of plasmids engineered for high-specificity editing of the Trp73 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Trp73. 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 Trp73 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 Trp73-disrupted clones.

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