TLR3 Double Nickase Plasmid (m): sc-431258-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TLR3 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
- TLR3 Double Nickase Plasmid (m) and TLR3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tlr3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TLR3 Double Nickase Plasmid (m) | sc-431258-NIC | 20 µg | $410.00 | |||
TLR3 Double Nickase Plasmid (m2) | sc-431258-NIC-2 | 20 µg | $410.00 |
Tlr3 encodes Toll-like receptor 3 (TLR3), an endosomal pattern-recognition receptor that detects double-stranded RNA produced during viral replication or released from damaged cells. Upon ligand binding, TLR3 signals predominantly through the TRIF adaptor to activate IRF3/IRF7 and NF-κB pathways, driving type I interferon production and inflammatory cytokine programs. This receptor contributes to innate immune sensing, dendritic cell maturation, and regulation of antiviral responses while intersecting with pathways controlling apoptosis and autophagy. Altered TLR3 activity has been linked to variation in susceptibility to viral infection and to dysregulated inflammation relevant to neuroinflammatory and autoimmune-like phenotypes in mouse models.
TLR3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tlr3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tlr3. 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 Tlr3 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 Tlr3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.