Date published: 2026-8-14

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MCM7 Double Nickase Plasmid (h): sc-400900-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • MCM7 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
  • MCM7 Double Nickase Plasmid (h) and MCM7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MCM7. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MCM7 Antibody (141.2): sc-9966
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    MCM7 Double Nickase Plasmid (h)

    sc-400900-NIC
    20 µg
    $410.00

    MCM7 Double Nickase Plasmid (h2)

    sc-400900-NIC-2
    20 µg
    $410.00

    MCM7 encodes a core subunit of the minichromosome maintenance (MCM2–7) helicase that licenses replication origins and drives DNA unwinding during S phase. As part of the pre-replication complex, MCM7 coordinates with CDC45 and GINS to support replication fork progression, genome stability, and cell-cycle checkpoint responses. Dysregulated MCM7 expression or replication licensing contributes to replication stress, aberrant proliferation, and chromosomal instability observed across multiple tumor types. MCM7 is also studied in contexts of DNA damage tolerance and proteostasis of replication factors during oncogene-induced stress.

    MCM7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MCM7 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MCM7. 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 MCM7 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 MCM7-disrupted clones.

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