Date published: 2026-8-15

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OAS3 Double Nickase Plasmid (m): sc-434225-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • OAS3 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
  • OAS3 Double Nickase Plasmid (m) and OAS3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Oas3. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: OAS3 Antibody (D-7): sc-398225
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    OAS3 Double Nickase Plasmid (m)

    sc-434225-NIC
    20 µg
    $410.00

    Mouse Oas3 encodes 2′-5′-oligoadenylate synthetase 3 (OAS3), an interferon-inducible cytosolic sensor of viral double-stranded RNA that catalyzes production of 2-5A to activate RNase L and promote degradation of viral and cellular RNA. This OAS3–RNase L axis integrates with type I interferon signaling, innate immune restriction, and stress-associated translational control, shaping antiviral responses and inflammatory outputs. Altered regulation of OAS family activity has been linked to dysregulated interferon programs and immune-mediated pathology, making OAS3 a useful entry point for dissecting host–pathogen interactions and innate immune signaling dynamics in mouse models.

    OAS3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Oas3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Oas3. 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 Oas3 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 Oas3-disrupted clones.

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