Date published: 2026-7-4

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ATG7 Double Nickase Plasmid (m): sc-428805-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ATG7 Double Nickase Plasmid (m) 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
  • ATG7 Double Nickase Plasmid (m) and ATG7 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Atg7. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ATG7 Antibody (B-9): sc-376212
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ATG7 Double Nickase Plasmid (m)

    sc-428805-NIC
    20 µg
    $410.00

    Mouse Atg7 encodes ATG7, an E1-like enzyme that activates ATG12 and LC3/ATG8 family proteins to drive ubiquitin-like conjugation reactions required for autophagosome formation. ATG7 functions centrally in macroautophagy, coordinating cargo sequestration and lysosomal turnover to maintain proteostasis and organelle quality control, including mitophagy. Through its role in nutrient sensing and cellular stress adaptation, ATG7 influences immune signaling, metabolism, and neurobiology, and its dysregulation is frequently studied in contexts such as neurodegeneration, inflammatory phenotypes, and cancer-related stress responses. Atg7-dependent autophagic flux is therefore a widely used readout for dissecting pathways that connect intracellular degradation to tissue homeostasis.

    ATG7 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Atg7 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Atg7. 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 Atg7 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 Atg7-disrupted clones.

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