Date published: 2026-7-10

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ARP Double Nickase Plasmid (m): sc-428989-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ARP 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
  • ARP Double Nickase Plasmid (m) and ARP Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Manf. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ARP Antibody (B-3): sc-515906
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ARP Double Nickase Plasmid (m)

    sc-428989-NIC
    20 µg
    $410.00

    Mesencephalic astrocyte-derived neurotrophic factor (Manf) is an endoplasmic reticulum–resident, stress-inducible protein that supports proteostasis and secretory pathway homeostasis in mammalian cells. In mouse, MANF is closely linked to the unfolded protein response and ER-associated quality control, modulating cellular survival programs under ER stress and perturbations in protein folding. Altered MANF signaling has been studied in contexts of neurodegeneration, metabolic stress, and inflammatory tissue injury, where ER stress and cell-type vulnerability intersect. These attributes make Manf a useful node for probing ER stress adaptation, secretory cell function, and stress-linked transcriptional remodeling in biomedical models.

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

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