Date published: 2026-7-13

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TLR9 Double Nickase Plasmid (m): sc-429882-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TLR9 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
  • TLR9 Double Nickase Plasmid (m) and TLR9 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tlr9. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TLR9 Antibody (5G5): sc-47723
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TLR9 Double Nickase Plasmid (m)

    sc-429882-NIC
    20 µg
    $410.00

    TLR9 Double Nickase Plasmid (m2)

    sc-429882-NIC-2
    20 µg
    $410.00

    Mouse Tlr9 encodes Toll-like receptor 9 (TLR9), an endosomal pattern-recognition receptor that detects unmethylated CpG motifs in microbial and self-derived DNA. Upon ligand engagement and endosomal maturation, TLR9 signals primarily through MYD88 to activate IRAK–TRAF6 cascades, inducing NF-κB and IRF7-dependent transcription of proinflammatory cytokines and type I interferons. This pathway coordinates innate immune activation in macrophages, dendritic cells, and B cells, shaping antigen presentation and adaptive immune polarization. Dysregulated TLR9 signaling has been implicated in inflammatory and autoimmune phenotypes, aberrant responses to nucleic acids, and tumor-immune interactions in mouse models.

    TLR9 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tlr9 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tlr9. 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 Tlr9 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 Tlr9-disrupted clones.

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